FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Tierney, E Bukelis, I Thompson, RE Ahmed, K Aneja, A Kratz, L Kelley, RI AF Tierney, Elaine Bukelis, Irena Thompson, Richard E. Ahmed, Khalid Aneja, Alka Kratz, Lisa Kelley, Richard I. TI Abnormalities of cholesterol metabolism in autism spectrum disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE Smith-Lemli-Opitz Syndrome; hypocholesterolemia; Autism Genetic Resource Exchange; Asperger disorder; pervasive developmental disorder ID LEMLI-OPITZ-SYNDROME; MASS-SPECTROMETRY; BIOSYNTHESIS AB Although Smith-Lemli-Opitz Syndrome (SLOS), a genetic condition of impaired cholesterol biosynthesis, is associated with autism [Tierney et al., 2001; Am J Med Genet 98:191-200.], the incidence of SLOS and other sterol disorders among individuals with autism spectrum disorders (ASD) is unknown. This study investigated (1) the incidence of biochemically diagnosed SLOS in blood samples from a cohort of subjects with ASD from families in which more than one individual had ASD and (2) the type and incidence of other sterol disorders in the same group. Using gas chromatography/mass spectrometry, cholesterol, and its precursor sterols were quantified in 100 samples from subjects with ASD obtained from the Autism Genetic Resource Exchange (AGRE) specimen repository. Although no sample had sterol levels consistent with SLOS, 19 samples had total cholesterol levels lower than 100 mg/dl, which is below the 5th centile for children over age 2 years. These findings suggest that, in addition to SLOS, there may be other disorders of sterol metabolism or homeostasis associated with ASD. (c) 2006 Wiley-Liss, Inc. C1 Kennedy Krieger Inst, Baltimore, MD 21211 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Genet, Baltimore, MD 21205 USA. RP Tierney, E (reprint author), Kennedy Krieger Inst, 3901 Greenspring Ave, Baltimore, MD 21211 USA. 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Trippe, Juan Stone, Janet Schmitz, Christoph TI Minicolumnar abnormalities in autism SO ACTA NEUROPATHOLOGICA LA English DT Review DE autistic disorder/pathology; child development disorders; pervasive; neocortex; neuropil; pyramidal cells ID HUMAN AUDITORY-CORTEX; PRIMARY VISUAL-CORTEX; HIGH-FUNCTIONING AUTISM; MATTER VOLUME INCREASE; RADIAL CELL COLUMNS; CEREBRAL-CORTEX; FRONTAL-CORTEX; CYTOARCHITECTONIC DEFINITION; DIAGNOSTIC INTERVIEW; SYNAPTIC CONNECTIONS AB Autism is characterized by qualitative abnormalities in behavior and higher order cognitive functions. Minicolumnar irregularities observed in autism provide a neurologically sound localization to observed clinical and anatomical abnormalities. This study corroborates the initial reports of a minicolumnopathy in autism within an independent sample. The patient population consisted of six age-matched pairs of patients (DSM-IV-TR and ADI-R diagnosed) and controls. Digital micrographs were taken from cortical areas S1, 4, 9, and 17. The image analysis produced estimates of minicolumnar width (CW), mean interneuronal distance, variability in CW (V (CW)), cross section of Nissl-stained somata, boundary length of stained somata per unit area, and the planar convexity. On average CW was 27.2 mu m in controls and 25.7 mu m in autistic patients (P = 0.0234). Mean neuron and nucleolar cross sections were found to be smaller in autistic cases compared to controls, while neuron density in autism exceeded the comparison group by 23%. Analysis of inter- and intracluster distances of a Delaunay triangulation suggests that the increased cell density is the result of a greater number of minicolumns, otherwise the number of cells per minicolumns appears normal. A reduction in both somatic and nucleolar cross sections could reflect a bias towards shorter connecting fibers, which favors local computation at the expense of inter-areal and callosal connectivity. C1 Univ Louisville, Dept Psychiat & Behav Sci, Louisville, KY 40292 USA. Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, Utrecht, Netherlands. Maastricht Univ, Dept Psychiat & Neuropsychol, Div Cellular Neurosci, Maastricht, Netherlands. Univ Wurzburg, Morphol Brain Res Unit, Wurzburg, Germany. Mt Sinai Sch Med, Dept Neurosci, New York, NY USA. EURON, Maastricht, Netherlands. RP Casanova, MF (reprint author), Univ Louisville, Dept Psychiat & Behav Sci, 500 S Preston St,Bldg 55A,Ste 217, Louisville, KY 40292 USA. 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Sideris, John Skinner, Martie Mankowski, Jean Bailey, Donald B., Jr. Roberts, Jane Mirrett, Penny TI Autistic behavior in children with fragile X syndrome: Prevalence, stability, and the impact of FMRP SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE fragile X syndrome; autism; fragile X mental retardation protein ID DSM-III-R; DEVELOPMENTAL DISORDERS; YOUNG MALES; SPECTRUM DISORDER; BOYS; COMMUNICATION; SCHEDULE; SYMPTOMS; PROFILE; INDIVIDUALS AB We examined autistic behavior in a cross-sectional sample of 179 children with fragile X syndrome (FXS) and a longitudinal subset of 116 children using the Childhood Autism Rating Scale (CARS) to (a) determine a prevalence of autistic behavior in FXS, (b) examine the stability of autistic ratings over time, and Q assess the association between the fragile X mental retardation protein (FMRP) and autistic behavior. Approximately 21% of the sample of 129 children (25.9% of boys) scored at or above the cutoff for autism. 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D., 2003, APPL LONGITUDINAL DA SKINNER M, 2004, AM J MED GENET A, V132, P25 Turk J., 1997, AUTISM, V1, P175, DOI 10.1177/1362361397012005 WING L, 1980, ACTA PSYCHIAT SCAND, V62, P241, DOI 10.1111/j.1600-0447.1980.tb07696.x NR 54 TC 161 Z9 163 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD SEP 1 PY 2006 VL 140A IS 17 BP 1804 EP 1813 DI 10.1002/ajmg.a.31286 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 080PL UT WOS:000240259900002 PM 16700053 ER PT J AU Budimirovic, DB Bukelis, I Cox, C Gray, RM Tierney, E Kaufmann, WE AF Budimirovic, Dejan B. Bukelis, Irena Cox, Christiane Gray, Robert M. Tierney, Elaine Kaufmann, Walter E. TI Autism spectrum disorder in fragile X syndrome: Differential contribution of adaptive socialization and social withdrawal SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE fragile X syndrome; autism; autism spectrum disorder; adaptive socialization; social withdrawal; social avoidance; social cognition ID DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; BEHAVIOR PROFILE; DOWN-SYNDROME; YOUNG MALES; CHILDREN; BOYS; MUTATION; PROTEIN; ADOLESCENTS AB The present study extends our previous work on characterizing the profile of social behavior abnormalities in boys with Fragile X (FraX) and autism spectrum disorder (ASD) using clinically oriented behavioral rating scales and standardized instruments. The goal was to further distinguish behavioral parameters contributing to the diagnostic classification of FraX + ASD. The Study design included two cohorts of boys with FraX (3-8 years), a larger main cohort for cross-sectional analyses (n = 56, 24 with ASD), and a longitudinal subset (n = 30, 11 with ASD) of the main cohort with up to 3 yearly observations. The focus was on the relative contribution of delayed adaptive socialization and social withdrawal, including item components of their corresponding rating instruments, to the diagnosis of ASD in boys with FraX. Using a combination of regression analyses, we demonstrated that: (1) as delayed socialization, social withdrawal is also a correlate of FraX + ASD; (2) items of social withdrawal scales representing avoidance were the main predictors of ASD status, particularly in older boys; (3) adaptive socialization skills reflecting rules of social behavior and recognition and labeling of emotions, linked to verbal reasoning abilities, were selectively associated with FraX+ASD; (4) adaptive socialization is the primary determinant over time of ASD status in boys with FraX; and (5) integrated adaptive socialization-social withdrawal models allow the identification of distinctive FraX+ASD subgroups. Altogether, our findings suggest that two distinct but interrelated social behavior abnormalities, one linked to impaired cognitive processes (delayed socialization) and the second one to disturbance in limbic circuits (avoidance), play a role in the development of ASD in boys with FraX. (c) 2006 Wiley-Liss, Inc. C1 Kennedy Krieger Inst, Ctr Genet Disorders Cognit & Behav, Baltimore, MD 21211 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Radiol & Radiol Sci, Baltimore, MD 21205 USA. RP Budimirovic, DB (reprint author), Kennedy Krieger Inst, Ctr Genet Disorders Cognit & Behav, 3901 Greenspring Ave,Room 208, Baltimore, MD 21211 USA. 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Elia, Maurizio Romano, Valentino Holbert, Sebastien Andres, Christian Chaabouni, Habiba Colleaux, Laurence Constant, Jacques Le Guennec, Jean-Yves Briault, Sylvain TI Association of a functional deficit of the BKCa channel, a synaptic regulator of neuronal excitability, with autism and mental retardation SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; CA2+-ACTIVATED K+ CHANNELS; POTASSIUM CHANNELS; LARGE-CONDUCTANCE; INDIVIDUALS; ETIOLOGY; MUTATION; RELEASE; COMPLEX; SCREEN AB Objective: Autism is a complex, largely genetic psychiatric disorder. In the majority of cases, the cause of autism is not known, but there is strong evidence for a genetic etiology. To identify candidate genes, the physical mapping of balanced chromosomal aberrations is a powerful strategy, since several genes have been characterized in numerous disorders. In this study, the authors analyzed a balanced reciprocal translocation arising de novo in a subject with autism and mental retardation. Method: The authors performed the physical mapping of the balanced 9q23/ 10q22 translocation by fluorescent in situ hybridization experiments using bacterial artificial chromosome clones covering the areas of interest. Results: Findings revealed that the KCNMA1 gene, which encodes the alpha- subunit of the large conductance Ca2+-activated K+ ( BKCa) channel, a synaptic regulator of neuronal excitability, is physically disrupted. Further molecular and functional analyses showed the haploinsufficiency of this gene as well as decreased activity of the coded BKCa channel. This activity can be enhanced in vitro by addition of a BKCa channel opener (BMS-204352). Further mutational analyses on 116 autistic subjects led to the identification of an amino acid substitution located in a highly conserved domain of the protein not found in comparison subjects. Conclusions: These results suggest a possible association between a functional defect of the BKCa channel and autistic disorder and raise the hypothesis that deficits in synaptic transmission may contribute to the physiopathology of autism and mental deficiency. C1 INSERM, U619, Lab Genet Chromosom, CHR Source, F-45067 Orleans, France. Univ Tours, Fac Med, Tours, France. Ctr Hosp, Unite Diagnost & Traitement Troubles Envahissants, Chartres, France. Hop Necker Enfants Malad, INSERM, U393, Paris, France. EPS Nicolle, Serv Malad Congenitales & Hereditaires, Tunis, Tunisia. Univ Rouen, UMR 6014, CNRS, Inst Rech Chim Organ Fine, Rouen, France. Razi Hosp, Serv Pedopsychiat, La Manouba, Tunisia. Lab Mol Psychiat & Neurogenet, Rome, Italy. IRCCS Oasi Maria SS, Neurol Serv, Troina, Italy. Univ Palermo, Dept Biopathol & Biomed Methodol, Palermo, Italy. RP Briault, S (reprint author), INSERM, U619, Lab Genet Chromosom, CHR Source, BP86709, F-45067 Orleans, France. 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Objective: To examine the relationship between advancing paternal age at birth of offspring and their risk of autism spectrum disorder (ASD). Design: Historical population-based cohort study. Setting: Identification of ASD cases from the Israeli draft board medical registry. Participants: We conducted a study of Jewish persons born in Israel during 6 consecutive years. Virtually all men and about three quarters of women in this cohort underwent draft board assessment at age 17 years. Paternal age at birth was obtained for most of the cohort; maternal age was obtained for a smaller subset. We used the smaller subset (n=132271) with data on both paternal and maternal age for the primary analysis and the larger subset (n=318506) with data on paternal but not maternal age for sensitivity analyses. Main Outcome Measures: Information on persons coded as having International Classification of Diseases, 10th Revision ASD was obtained from the registry. The registry identified 110 cases of ASD (incidence, 8.3 cases per 10000 persons), mainly autism, in the smaller subset with complete parental age data. Results: There was a significant monotonic association between advancing paternal age and risk of ASD. Offspring ofmen 40 years or olderwere 5.75 times (95% confidence interval, 2.65-12.46; P <.001) more likely to have ASD compared with offspring of menyounger than 30 years, after controlling for year of birth, socioeconomic status, and maternal age. Advancing maternal age showed no association with ASD after adjusting for paternal age. Sensitivity analyses indicated that these findings were not the result of bias due to missing data on maternal age. Conclusions: Advanced paternal age was associated with increased risk of ASD. Possible biological mechanisms include de novo mutations associated with advancing age or alterations in genetic imprinting. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. 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Nine social pictures with human beings (including two pictures of cat mask), and 3 nonsocial pictures of objects were presented for 5 seconds. Saccadic movements and fixation were recorded with equipment EyeGaze((R)) (LC Technologies Inc.). Results: PDDG (mean=292.73, SE=67.62) presented longer duration of saccadic movements for social pictures compared to CG (mean=136.06, SE=14.01) (p=0.04). The CG showed a higher number of fixations in the picture 7 (a women using a cat mask, with the eyes erased) (CG: mean=3.40; PDDG: mean=1.80; p=0.007). Conclusion: The results suggest differences in strategies that PDD explore human picture. Moreover, these strategies seem not to be affected by the lack of expected part of the face (the eyes). C1 Mackenzie Presbyterian Univ, Dev Disorder Program, Sao Paulo, Brazil. RP Mercadante, MT (reprint author), Mackenzie Presbyterian Univ, Dev Disorder Program, Sao Paulo, Brazil. 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Neuro-Psiquiatr. PD SEP PY 2006 VL 64 IS 3A BP 559 EP 562 DI 10.1590/S0004-282X2006000400003 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 085OU UT WOS:000240614200003 PM 17119790 ER PT J AU Goin-Kochel, RP Mackintosh, VH Myers, BJ AF Goin-Kochel, Robin P. Mackintosh, Virginia H. Myers, Barbara J. TI How many doctors does it take to make an autism spectrum diagnosis? SO AUTISM LA English DT Article DE autism spectrum; diagnosis; diagnostic age; parent satisfaction ID DEVELOPMENTAL DELAYS; DISORDER; CHILDREN; IDENTIFICATION; DIFFICULTIES; CARE AB Parents of children with pervasive developmental disorders (n = 494) were surveyed to determine their level of satisfaction with the process of getting an autism spectrum diagnosis. Participants in this web-based study (mean age = 37.8 years) came from five countries and reported on children with an average age of 8.3 years (range = 1.7 to 22.1). All children had a diagnosis of either autism (59.9%), Asperger syndrome (23.5%), or PDD-NOS (16.6%). Higher levels of parental education and income were associated with earlier diagnosis and greater satisfaction with the diagnostic process. Parents were more satisfied with the diagnostic process when they saw fewer professionals to get the diagnosis and when the children received the diagnoses at younger ages. C1 Virginia Commonwealth Univ, Richmond, VA USA. Baylor Coll Med, Houston, TX 77030 USA. RP Goin-Kochel, RP (reprint author), Texas Childrens Hosp, 6621 Fannin St CC1560, Houston, TX 77030 USA. 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Patrick, Patricia A. Edwards, Karen S. Brand, Donald A. TI Parental beliefs about autism - Implications for the treating physician SO AUTISM LA English DT Article DE alternative medicine; autism diagnosis; autism etiology; autism therapy; complementary medicine ID DEVELOPMENTAL DELAYS; ALTERNATIVE MEDICINE; SPECTRUM DISORDERS; YOUNG-CHILDREN; COMPLEMENTARY; PREVALENCE; CHECKLIST; TODDLERS AB This study investigated parental beliefs about the etiology, diagnosis, and treatment of autism spectrum disorders. Sixty-two families of affected children completed a questionnaire asking when the parent first noticed developmental or behavioral problems, when they were told the diagnosis, how confident they were about the ability of their child's physician to recognize autism, whether they believed anything specific might have caused their child's autism, and what medications and complementary or alternative therapies they had tried. Two-thirds of parents suspected a specific cause, and three-quarters questioned their physician's ability. Parents who perceived a greater delay in diagnosis or who had tried more different therapies both tended to have less confidence in their physician (p = 0.20 and p = 0.07, respectively). Physicians should inquire about parental beliefs concerning etiology, learn what treatments the children are receiving, perform screening at the 18 month visit, and make referrals for further evaluation as soon as a child begins to exhibit signs suggestive of autism. C1 New York Med Coll, Dept Pediat, Valhalla, NY 10595 USA. RP Harrington, JW (reprint author), New York Med Coll, Dept Pediat, 312 Munger Pavillon, Valhalla, NY 10595 USA. EM John_Harrington@nymc.edu CR Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Hyman SL, 2000, CONT PEDIAT, V17, P101 Levy SE, 2003, J DEV BEHAV PEDIATR, V24, P418, DOI 10.1097/00004703-200312000-00003 Levy SE, 2003, PEDIATR ANN, V32, P685 Mailick Seltzer M., 2000, INT REV RES MENTAL R, V23 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 McGuire JK, 2000, PEDIATRICS, V105, DOI 10.1542/peds.105.2.e18 Nickel RE, 1996, INFANT YOUNG CHILD, V8, P29 Robins DL, 2001, J AUTISM DEV DISORD, V31, P131, DOI 10.1023/A:1010738829569 Sandler AD, 2001, PEDIATRICS, V107, P598 Scambler D, 2001, J AM ACAD CHILD PSY, V40, P1457, DOI 10.1097/00004583-200112000-00017 Sices L, 2004, PEDIATRICS, V113, P274, DOI 10.1542/peds.113.2.274 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 16 TC 25 Z9 25 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2006 VL 10 IS 5 BP 452 EP 462 DI 10.1177/1362361306066609 PG 11 WC Psychology, Developmental SC Psychology GA 095AC UT WOS:000241279600003 PM 16940312 ER PT J AU Dale, E Jahoda, A Knott, F AF Dale, Emily Jahoda, Andrew Knott, Fiona TI Mothers' attributions following their child's diagnosis of autistic spectrum disorder - Exploring links with maternal levels of stress, depression and expectations about their child's future SO AUTISM LA English DT Article DE attributions; autistic spectrum disorder (ASD); mothers ID ASPERGER-SYNDROME; FAMILIES; PARENTS; INTERVENTION; GUIDELINES; PREDICTORS; BELIEFS AB Although the impact of autism spectrum disorders (ASDs) on the family is well recognized, the way mothers attempt to make sense of the diagnosis is largely unexplored. However, in other disabilities, attributions have been shown to predict a variety of outcomes including maternal wellbeing and engagement in treatment. Using Weiner's (198S) three-dimensional model, 16 mothers were interviewed to examine the nature and impact of their beliefs about their child's ASD using semi-structured interviews and measures of depression, parenting stress and expectations for their child's future. The findings suggested that mothers made a diverse and complex range of attributions that were consistent with Weiner's dimensions of locus of cause, stability and controllability. The nature of their attributions reflected particular difficulties associated with ASDs, such as uncertainties regarding cause and prognosis. Taking account of mothers' search for meaning will better enable professionals to support families following diagnosis. C1 Univ Reading, Reading RG6 2AH, Berks, England. Univ Glasgow, Glasgow G12 8QQ, Lanark, Scotland. RP Dale, E (reprint author), Northumberland Tyne & Wear NHS Trust, Newcastle Child & Adolescent Mental Hlth Serv, Fleming Nuffield Unit, Newcastle Upon Tyne NE2 3AE, Tyne & Wear, England. 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Trivedi, Madhukar H. Garver, Carolyn R. Grannemann, Bruce D. Andrews, Alonzo A. Savla, Jayshree S. Johnson, Danny G. Mehta, Jyutika A. Schroeder, Jennifer L. TI The pattern of sensory processing abnormalities in autism SO AUTISM LA English DT Article DE autism; sensory processing; Sensory Profile ID SPECTRUM DISORDERS; SYMPTOMS; DEFENSIVENESS; CHILDREN; PROFILE AB The study was undertaken to evaluate the nature of sensory dysfunction in persons with autism. The cross-sectional study examined auditory, visual, oral, and touch sensory processing, as measured by the Sensory Profile, in 104 persons with a diagnosis of autism, 3-56 years of age, gender- and age-matched to community controls. Persons with autism had abnormal auditory, visual, touch, and oral sensory processing that was significantly different from controls. This finding was also apparent when the high and low thresholds of these modalities were examined separately. At later ages for the group with autism, lower levels of abnormal sensory processing were found, except for low threshold touch, which did not improve significantly. There was a Significant interaction in low threshold auditory and low threshold visual, suggesting that the two groups change differently over time on these variables. These results suggest that sensory abnormalities in autism are global in nature (involving several modalities) but have the potential to improve with age. C1 Univ Texas, SW Med Ctr, Dept Psychiat, Dallas, TX 75390 USA. Autism Treatment Ctr, Dallas, TX USA. RP Kern, JK (reprint author), Univ Texas, SW Med Ctr, Dept Psychiat, 6363 Forest Pk Rd,Suite 13-354, Dallas, TX 75390 USA. 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Bosseler, Alexis TI Read my lips - The importance of the face in a computer-animated tutor for vocabulary learning by children with autism SO AUTISM LA English DT Article DE autism; computer animation; language learning; vocabulary tutor ID LANGUAGE IMPAIRMENTS; EVOKED-RESPONSES; RECOGNITION; ACQUISITION; DESIGN AB A computer-animated tutor, Baldi, has been successful in teaching vocabulary and grammar to children with autism and those with hearing problems. The present study assessed to what extent the face facilitated this learning process relative to the voice alone. Baldi was implemented in a Language Wizard/Tutor, which allows easy creation and presentation of a vocabulary lesson involving the association of pictures and spoken words. The lesson plan included both the receptive identification of pictures and the production of spoken words. A within-subject design with five children with autism followed an alternating treatment in which each child continuously learned to criterion sets of words with and without the face. The rate of learning was significantly faster and the retention was better with the face. The research indicates that at least some children with autism benefit from the face in learning new language within an automated program. C1 Univ Calif Santa Cruz, Dept Psychol, Santa Cruz, CA 95064 USA. RP Massaro, DW (reprint author), Univ Calif Santa Cruz, Dept Psychol, Santa Cruz, CA 95064 USA. 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In this study, disability and support characteristics associated with variations in the level of quality of life among adults with ASD are identified, using self-report measures. Fifty-eight high-functioning adults with ASD participated in the study. The results of a multiple linear regression analysis reveal that support characteristics are related to quality of life in adults with ASD, whereas disability characteristics are not. The R-2 effect size (0.620) is large and significant. The results reinforce the significance of an available supportive social network, the importance of a substantial needs assessment and effective professional support. C1 Univ Ghent, Dept Expt Clin & Hlth Psychol, Res Grp Dev Disorders, B-9000 Ghent, Belgium. RP Renty, J (reprint author), Univ Ghent, Dept Expt Clin & Hlth Psychol, Res Grp Dev Disorders, Henri Dunantlaan 2, B-9000 Ghent, Belgium. 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Viola, Angele TI In vivo characterization of brain morphometric and metabolic endophenotypes in three inbred strains of mice using magnetic resonance techniques SO BEHAVIOR GENETICS LA English DT Article DE mouse strains; magnetic resonance imaging (MRI); magnetic resonance spectroscopy (MRS); brain; neurochemistry; psychiatry; neurology ID QUANTITATIVE TRAIT LOCI; CENTRAL-NERVOUS-SYSTEM; HUMAN-GENOME-PROJECT; ALZHEIMERS-DISEASE; N-ACETYLASPARTATE; RELAXATION-TIMES; CRITICAL REGION; DOWN-SYNDROME; MOUSE MODEL; SPECTROSCOPY AB C57BL/6J, FVB/N and 129/SvJ mice are commonly used as background strains to engineer genetic models of brain pathologies and psychiatric disorders. Magnetic resonance imaging (MRI) and spectroscopy provide alternative approaches to neuroanatomy, histology and neurohistochemistry for investigating the correlation between genes and brain neuroanatomy and neurometabolism in vivo. We used these techniques to non-invasively characterize the cerebral morphologic and metabolic endophenotypes of inbred mouse strains commonly used in neurological and behavioral research. We observed a great variability in the volume of ventricles and of structures involved in cognitive function (cerebellum and hippocampus) among these strains. In addition, distinct metabolic profiles were evidenced with variable levels of N-acetylaspartate, a neuronal marker, and of choline, a compound found in membranes and myelin. Besides, significant differences in high-energy phosphates and phospholipids were detected. Our findings demonstrate the great morphologic and metabolic heterogeneity among C57BL/6J, FVB/N and 129/SvJ mice. They emphasize the importance of selecting the appropriate genetic background for over-expressing or silencing a gene and provide some directions for modeling symptoms that characterize psychiatric disorders such as autism, schizophrenia and depression. 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Genet. PD SEP PY 2006 VL 36 IS 5 BP 732 EP 744 DI 10.1007/s10519-006-9077-4 PG 13 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 071HG UT WOS:000239589700011 PM 16710778 ER PT J AU Kana, RK Keller, TA Cherkassky, VL Minshew, NJ Just, MA AF Kana, Rajesh K. Keller, Timothy A. Cherkassky, Vladimir L. Minshew, Nancy J. Just, Marcel Adam TI Sentence comprehension in autism: thinking in pictures with decreased functional connectivity SO BRAIN LA English DT Article DE autism; cortical connectivity; high imagery; low imagery; functional MRI ID DEVELOPMENTAL LANGUAGE DISORDER; HUMAN CORPUS-CALLOSUM; ASPERGER-SYNDROME; WORKING-MEMORY; CHILDREN; BRAIN; COMMUNICATION; INDIVIDUALS; SUPERIOR; TASK AB Comprehending high-imagery sentences like The number eight when rotated 90 degrees looks like a pair of eyeglasses involves the participation and integration of several cortical regions. The linguistic content must be processed to determine what is to be mentally imaged, and then the mental image must be evaluated and related to the sentence. A theory of cortical underconnectivity in autism predicts that the interregional collaboration required between linguistic and imaginal processing in this task would be underserved in autism. This functional MRI study examined brain activation in 12 participants with autism and 13 age- and IQ-matched control participants while they processed sentences with either high- or low-imagery content. The analysis of functional connectivity among cortical regions showed that the language and spatial centres in the participants with autism were not as well synchronized as in controls. In addition to the functional connectivity differences, there was also a group difference in activation. In the processing of low-imagery sentences (e.g. Addition, subtraction and multiplication are all moth skills), the use of imagery is not essential to comprehension. Nevertheless, the autism group activated parietal and occipital brain regions associated with imagery for comprehending both the low and high-imagery sentences, suggesting that they were using mental imagery in both conditions. In contrast, the control group showed imagery-related activation primarily in the high-imagery condition. The findings provide further evidence of underintegration of language and imagery in autism (and hence expand the understanding of underconnectivity) but also show that people with autism are more reliant on visualization to support language comprehension. C1 Carnegie Mellon Univ, Ctr Cognit Brain Imaging, Dept Psychol, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA. Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA USA. RP Kana, RK (reprint author), Carnegie Mellon Univ, Ctr Cognit Brain Imaging, Dept Psychol, Pittsburgh, PA 15213 USA. 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The aim of this study was to evaluate the prevalence of brain abnormalities in a group of young children with developmental disorders, specifically including children that came to the attention of a child psychiatrist before the age of 3 years. Methods. Forty-five children participated in an MR study (mean age 43 months, SD = 12, four females). The study design was approved by the local Medical Ethical Review Board. All parents gave written informed consent. Scans were independently assessed by two board-certified radiologists for malformations of gray and white matter. Results. Cohen's kappa for the consensus between the two raters was 0.79. In 22 children (49%) abnormalities were reported. Four patients (8.5%) had an arachnoid cyst. One female was diagnosed with a Chiari I malformation. Three children show enlarged Virchow-Robin spaces, an increased occurrence when compared to the normal population. Conclusions. A high rate of intracranial abnormalities was found in this study. Radiological findings do not contribute to the diagnosis of developmental disorders. However, young children with developmental disorders may not be able to express discomfort associated with brain abnormalities, such as a Chiari I malformation. Given the high prevalence of abnormalities in this sample neuroimaging may be a useful tool in clinically assessing children with developmental disorders. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Utrecht, Rudolf Magnus Inst Neurosci, Dept Child & Adolescent Psychiat, Med Ctr, Utrecht, Netherlands. Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands. Univ Utrecht, Med Ctr, Dept Radiol, Utrecht, Netherlands. UMC St Radboud, Dept Psychiat, Acad Ctr Child & Adolescent Psychiat, Nijmegen, Netherlands. RP Zeegers, M (reprint author), Univ Utrecht, Rudolf Magnus Inst Neurosci, Dept Child & Adolescent Psychiat, Med Ctr, Utrecht, Netherlands. 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PD SEP PY 2006 VL 28 IS 8 BP 495 EP 499 DI 10.1016/j.braindev.2006.02.006 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 074UO UT WOS:000239837500004 PM 16616445 ER PT J AU McGraw-Hunter, M Faw, GD Davis, PK AF McGraw-Hunter, M. Faw, G. D. Davis, P. K. TI The use of video self-modelling and feedback to teach cooking skills to individuals with traumatic brain injury: A pilot study SO BRAIN INJURY LA English DT Article DE modelling; video self-modelling; cooking; activities of daily living ID CHILDREN; AUTISM; REHABILITATION; SETTINGS AB Objective: To evaluate the effectiveness of video self-modelling plus prompting and feedback to teach a cooking skill to people with traumatic brain injury (TBI) and to examine skill generalization to a novel food item. Research design: Multiple probe across participants. Methods and procedures: Four individuals with TBI received instruction in cooking. They watched videotapes of themselves cooking and practiced that skill while receiving prompts and feedback. Treatment effects were evaluated by comparing performance before, during and after training and at a 2 and 4 week follow-up. Additionally, cooking performance on a novel food item was examined. Main outcomes and results: Three of the four individuals achieved criterion performance within four training sessions. Those individuals also substantially maintained their skills 2 and 4 weeks following training and generalized their skills to a novel food item. Conclusions: Video self-modelling plus prompting and feedback appears to be an effective treatment for teaching simple cooking skills to individuals with TBI. Further research should examine whether the video alone is sufficient for skill acquisition and evaluate the effectiveness of video self-modelling to teach other skills. C1 So Illinois Univ, Inst Rehabil, Carbondale, IL 62901 USA. Ctr Comprehens Serv, Carbondale, IL USA. 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PD SEP PY 2006 VL 20 IS 10 BP 1061 EP 1068 DI 10.1080/02699050600912163 PG 8 WC Neurosciences; Rehabilitation SC Neurosciences & Neurology; Rehabilitation GA 093FA UT WOS:000241152100008 PM 17060139 ER PT J AU Akbarian, S Huang, HS AF Akbarian, Schahram Huang, Hsien-Sung TI Molecular and cellular mechanisms of altered GAD1/GAD67 expression in schizophrenia and related disorders SO BRAIN RESEARCH REVIEWS LA English DT Review DE schizophrenia; interneuron; GABA; brain-derived neurotrophic factor; glutamic acid decarboxylase; single nucleotide polymorphisms ID GLUTAMIC-ACID DECARBOXYLASE; GAMMA-AMINOBUTYRIC-ACID; MESSENGER-RNA EXPRESSION; DORSOLATERAL PREFRONTAL CORTEX; CHILDHOOD-ONSET SCHIZOPHRENIA; MAJOR DEPRESSIVE DISORDER; ANTERIOR CINGULATE CORTEX; CALCIUM-BINDING PROTEINS; HETEROZYGOUS REELER MICE; BIPOLAR DISORDER AB The 67 and 65 kDa isoforms of glutamic acid decarboxylase, the key enzymes for GABA biosynthesis, are expressed at altered levels in postmortem brain of subjects diagnosed with schizophrenia and related disorders, including autism and bipolar illness. The predominant finding is a decrease in GAD67 mRNA levels, affecting multiple brain regions, including prefrontal and temporal cortex. Postmortem studies, in conjunction with animal models, identified several mechanisms that contribute to the dysregulation of GAD67 in cerebral cortex. These include disordered connectivity formation during development, abnormal expression of Reelin and neural cell adhesion molecule (NCAM) glycoproteins, defects in neurotrophin signaling and alterations in dopaminergic and glutamatergic neurotransmission. These mechanisms are likely to operate in conjunction with genetic risk factors for psychosis, including sequence polymorphisms residing in the promoter of GAD1 (2q31), the gene encoding GAD67. We propose an integrative model, with multiple molecular and cellular mechanisms contributing to transcriptional dysregulation of GAD67 and cortical dysfunction in psychosis. (c) 2006 Elsevier B.V. All rights reserved. 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On the basis of an hypothesis about the restricted social awareness of children and adolescents with autism, we predicted that there would be little differentiation between their drawings of themselves and other people. To test this prediction, we investigated a group of children and adolescents with autism and a group with learning difficulties but not autism (N = 14 per group) who were individually matched for both chronological age and verbal mental age. Participants with autism mostly drew human figures that were little distinguished from one another, but introduced clear contrasts among their houses, whereas most of those with learning difficulties drew distinctive human figures as well as houses. These different profiles of performance occurred despite similarities in the numbers and kinds of feature included in the drawings, and the individuality of participants' drawing styles. 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Snyder, Josh Tager-Flusberg, Helen TI Anatomical differences in the mirror neuron system and social cognition network in autism SO CEREBRAL CORTEX LA English DT Review DE autism; cortical thickness; empathy; mirror neuron system ID PERVASIVE DEVELOPMENTAL DISORDERS; MAGNETIC-RESONANCE IMAGES; SUPERIOR TEMPORAL SULCUS; HIGH-FUNCTIONING AUTISM; HEAD CIRCUMFERENCE; ASPERGERS-SYNDROME; CEREBRAL-CORTEX; MOTOR FACILITATION; SPECTRUM DISORDER; BRAIN STRUCTURE AB Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with impaired social and emotional skills, the anatomical substrate of which is still unknown. In this study, we compared a group of 14 high-functioning ASD adults with a group of controls matched for sex, age, intelligence quotient, and handedness. We used an automated technique of analysis that accurately measures the thickness of the cerebral cortex and generates cross-subject statistics in a coordinate system based on cortical anatomy. We found local decreases of gray matter in the ASD group in areas belonging to the mirror neuron system (MINIS), argued to be the basis of empathic behavior. Cortical thinning of the MNS was correlated with ASD symptom severity. Cortical thinning was also observed in areas involved in emotion recognition and social cognition. These findings suggest that the social and emotional deficits characteristic of autism may reflect abnormal thinning of the MNS and the broader network of cortical areas subserving social cognition. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA. Harvard Univ, MIT, Div Hlth Sci & Technol, Cambridge, MA 02139 USA. Boston Univ, Sch Med, Boston, MA 02118 USA. RP Hadjikhani, N (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Bldg 36,1st St,Room 417, Charlestown, MA 02129 USA. 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Cortex PD SEP PY 2006 VL 16 IS 9 BP 1276 EP 1282 DI 10.1093/cercor/bh069 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 072QV UT WOS:000239689000005 PM 16306324 ER PT J AU Taylor, B AF Taylor, B. TI Vaccines and the changing epidemiology of autism SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE autism; epidemiology; immunization; pervasive developmental disorders; prevalence data ID PERVASIVE DEVELOPMENTAL DISORDERS; CAUSAL ASSOCIATION; RUBELLA VACCINE; THIMEROSAL EXPOSURE; PRESCHOOL-CHILDREN; SPECTRUM DISORDER; MMR VACCINATION; UNITED-KINGDOM; NO EVIDENCE; PREVALENCE AB Background:The epidemiology of autism has been rather confusing, with very variable published prevalence figures and no clear incidence data. The cause of autism is unclear; vaccines have been incriminated. Methods:Literature review and interpretation. Results:The recorded prevalence of autism has increased considerably in recent years. This reflects greater recognition, with changes in diagnostic practice associated with more trained diagnosticians; broadening of diagnostic criteria to include a spectrum of disorder; a greater willingness by parents and educationalists to accept the label (in part because of entitlement to services); and better recording systems, among other factors. The cause(s) of autism remains unclear. There is a strong genetic component which, along with prenatally determined neuro-anatomical/biochemical changes, makes any post-natal 'cause' unlikely. Conclusions:There has (probably) been no real increase in the incidence of autism. There is no scientific evidence that the measles, mumps and rubella (MMR) vaccine or the mercury preservative used in some vaccines plays any part in the aetiology or triggering of autism, even in a subgroup of children with the condition. C1 Royal Free & Univ Coll, Sch Med, London NW3 2PF, England. RP Taylor, B (reprint author), Royal Free & Univ Coll, Sch Med, UCL Hampstead, London NW3 2PF, England. EM brent.taylor@medschool.ucl.ac.uk CR Andrews N, 2004, PEDIATRICS, V114, P584, DOI 10.1542/peds.2003-1177-L Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Committee on Safety of Medicines, 1999, CURRENT PROBLEMS PHA, V25, P9 Croen LA, 2003, J AUTISM DEV DISORD, V33, P227, DOI 10.1023/A:1022964132203 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Department of Developmental Services, 1999, CHANG POP PERS AUT P Department of Developmental Services, 2003, AUT SPECTR DIS CHANG EYPASCH E, 1995, BRIT MED J, V311, P619 Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 GERSHON M, 2002, REVISIONES VACUNAS, V2, P156 Gillberg C., 1998, AUTISM, V2, P423, DOI 10.1177/1362361398024007 GILLBERG C, 1984, J CHILD PSYCHOL PSYC, V25, P35, DOI 10.1111/j.1469-7610.1984.tb01717.x GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Gurney JG, 2003, ARCH PEDIAT ADOL MED, V157, P622, DOI 10.1001/archpedi.157.7.622 Heron J, 2004, PEDIATRICS, V114, P577, DOI 10.1542/peds.2003-1176-L Heussler H, 2001, BRIT MED J, V323, P633 Honda H, 2005, J CHILD PSYCHOL PSYC, V46, P572, DOI 10.1111/j.1469-7610.2005.01425.x Jick H, 2003, PHARMACOTHERAPY, V23, P1524, DOI 10.1592/phco.23.15.1524.31955 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Lingam R, 2003, ARCH DIS CHILD, V88, P666, DOI 10.1136/adc.88.8.666 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 McCormick M, 2004, REPORT I MED IMMUNIZ *MIND I, 2002, EP AUT CAL REP LEG P MURCH SM, 2004, LANCET, V363, P75 Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Parker SK, 2004, PEDIATRICS, V114, P793, DOI 10.1542/peds.2004-0434 Peltola H, 1998, LANCET, V351, P1327, DOI 10.1016/S0140-6736(98)24018-9 Smeeth L, 2004, LANCET, V364, P963, DOI 10.1016/S0140-6736(04)17020-7 Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 1999, LANCET, V354, P949, DOI 10.1016/S0140-6736(05)75696-8 NR 37 TC 16 Z9 17 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD SEP PY 2006 VL 32 IS 5 BP 511 EP 519 DI 10.1111/j.1365-2214.2006.00655.x PG 9 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 071WU UT WOS:000239635400002 PM 16919130 ER PT J AU Wigram, T Gold, C AF Wigram, T. Gold, C. TI Music therapy in the assessment and treatment of autistic spectrum disorder: clinical application and research evidence SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE music therapy; assessment; research evidence; autism; clinical reports ID JOINT ATTENTION; CHILDREN; SKILLS; METAANALYSIS; ADOLESCENTS; BEHAVIORS; IMITATION AB Background:Children and adolescents with autistic spectrum disorder (ASD) presenting with significant limitations in conventional forms of verbal and non-verbal communication are found to respond positively to music therapy intervention involving both active, improvizational methods and receptive music therapy approaches. Improvizational musical activity with therapeutic objectives and outcomes has been found to facilitate motivation, communication skills and social interaction, as well as sustaining and developing attention. The structure and predictability found in music assist in reciprocal interaction, from which tolerance, flexibility and social engagement to build relationships emerge, relying on a systematic approach to promote appropriate and meaningful interpersonal responses. Results:Published reports of the value and effectiveness of music therapy as an intervention for children with ASD range from controlled studies to clinical case reports. Further documentation has emphasized the role music therapy plays in diagnostic and clinical assessment. Music therapy assessment can identify limitations and weaknesses in children, as well as strengths and potentials. Research evidence from a systematic review found two randomized controlled trials that examined short-term effects of structured music therapy intervention. Significant effects were found in these studies even with extremely small samples, and the findings are important because they demonstrate the potential of the medium of music for autistic children. Case series studies were identified that examined the effects of improvizational music therapy where communicative behaviour, language development, emotional responsiveness, attention span and behavioural control improved over the course of an intervention of improvizational music therapy. C1 Univ Aalborg, Inst Musik & Musikterapi, Fac Humanities, Aalborg, Denmark. Sogn Fjordane Univ, Fac Hlth Studies, N-6851 Sogndal, Norway. RP Wigram, T (reprint author), Univ Aalborg, Inst Musik & Musikterapi, Fac Humanities, Aalborg, Denmark. 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W., 1998, NORD J MUSIC THER, V7, P40 SCHOGLER BW, 2003, P 5 TRIENN C EUR SOC SCHUMACHER A, 1999, NORDIC J MUSIC THERA, V8, P188 Siegel D. J., 1999, DEV MIND NEUROBIOLOG Sigman M., 1995, JOINT ATTENTION ITS, P189 Stern D., 1985, INTERPERSONAL WORLD TREVARTHEN C, 2002, ENFANCE, V1, P86 Trevarthen C, 2001, INFANT MENT HEALTH J, V22, P95, DOI 10.1002/1097-0355(200101/04)22:1<95::AID-IMHJ4>3.0.CO;2-6 Trevarthen C., 1999, MUSIC SCI, P155 Trevarthen C., 1996, CHILDREN AUTISM DIAG Whipple J, 2004, J MUSIC THER, V41, P90 WIGRAM T, 2002, COMPREHENSIVE GUIDE, P145 Wigram T., 2004, IMPROVISATION METHOD Wigram T., 1999, NORD J MUSIC THER, V8, P6 Wigram T., 2002, BRIT J MUSIC THERAPY, V16, P11 Wigram T., 2000, MUSIC THERAPY PERSPE, V18, P13 NR 50 TC 24 Z9 26 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD SEP PY 2006 VL 32 IS 5 BP 535 EP 542 DI 10.1111/j.1365-2214.2006.00615.x PG 8 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 071WU UT WOS:000239635400004 PM 16919132 ER PT J AU Jones, G AF Jones, G. TI Department for Education and Skills/Department of Health Good Practice Guidance on the education of children with autistic spectrum disorder SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE autism; education; national guidance ID EARLY INTERVENTION; ISSUES AB Currently, it is held by many that educational interventions are those most likely to make a significant difference to the prognosis and well-being of a child with an autistic spectrum disorder (ASD). Yet, decision making about educational interventions and provision in ASD is often based on beliefs, tradition and assumptions, rather than on empirical evidence. This can lead to inappropriate or ineffective provision and can cause confusion and conflict between and within professional groups and parents. Little rigorous research evidence exists to guide decisions for children with ASD. This is true for educational practice generally, and for children with other special educational needs. Practitioners and parents alike are keen for good information on how best to educate children with ASD. It was against this background that the Department for Education and Skills (DfES) and Department of Health (DoH) convened a working group of experienced practitioners and parents to produce the 'Good Practice Guidance on ASDs'. This paper explores the need for the DfES/DoH Guidance, describes its structure and content and then suggests why research evidence is sparse and how future research might be enhanced to inform practice. C1 Univ Birmingham, Sch Educ, Birmingham B15 2TT, W Midlands, England. RP Jones, G (reprint author), Univ Birmingham, Sch Educ, Birmingham B15 2TT, W Midlands, England. EM g.e.jones@bham.ac.uk CR *ADV COMM SUPPL ED, 1984, TEACH TRAIN SPEC ED Ainscow M., 1997, BRIT J SPECIAL ED, V24, P3, DOI 10.1111/1467-8527.00002 BALFE P, 2001, GOOD AUTISM PRACTICE, V2, P75 Baron-Cohen S., 2000, UNDERSTANDING OTHERS Charman T, 2003, AUTISM, V7, P217 DANIELS H, 1998, EMOTIONAL BEHAV DIFF Dawson G., 1997, EFFECTIVENESS EARLY, P307 *DFES, 2002, AUT SPECTR DIS GOOD *DFES, 2001, COD PRACT SPEC ED NE Dyson A., 2002, SYSTEMATIC REV EFFEC EVANS J, 2001, 22 NFER Freeman BJ, 1997, J AUTISM DEV DISORD, V27, P641, DOI 10.1023/A:1025850715183 Frith U., 2003, AUTISM EXPLAINING EN Garner P., 1996, BRIT J SPECIAL ED, V23, P176, DOI 10.1111/j.1467-8578.1996.tb00972.x GERLAND G, 1997, REAL PERSON GERSCH IS, 1996, ED CHILD PSYCHOLA, V13, P31 GRAY C, 1994, SOCIAL STORY BOOK Guralnick MJ., 1997, EFFECTIVENESS EARLY Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Helps S, 1999, AUTISM, V3, P287, DOI 10.1177/1362361399003003006 Howlin P, 1998, CHILDREN AUTISM ASPE Howlin P, 1998, J CHILD PSYCHOL PSYC, V39, P307, DOI 10.1017/S0021963097002138 JONES G, 1995, UNPUB DESCRIPTIVE CO Jones G., 2002, ED PROVISION CHILDRE Jordan R, 2001, AUTISM SEVERE LEARNI Jordan R, 1998, ED INTERVENTIONS CHI JORDAN R, 1995, UNDERSTANDING TECHNI Koegel LK, 1997, J AUTISM DEV DISORD, V27, P233, DOI 10.1023/A:1025894213424 Lawson W., 2001, UNDERSTANDING WORKIN LEWIS J, 1999, GOOD AUTISM PRACTICE, P76 LINDSAY G, 2007, VALUES PRACTICE SPEC, P27 Lord C, 2000, J AUTISM DEV DISORD, V30, P393, DOI 10.1023/A:1005591205002 McGregor E, 2001, AUTISM, V5, P189 Mesibov GB, 2003, ACCESSING CURRICULUM MILLER C, 1996, CROSSROADS SEN TEACH, P35 *MRC, 2001, REV AUT RES EP CAUS *NAS, 2003, NAT ACT PLAN CHILDR NORWICH B, 2002, LEA INCLUSION TRENDS NORWICH B, 1994, CURRICULUM STUDIES, V2, P289 PARKS SL, 1983, J AUTISM DEV DISORD, V25, P415 Powell S, 1997, AUTISM LEARNING GUID PREECE D, 2000, GOOD AUTISM PRACTICE, V1, P42 Prizant BM, 1999, J ASSOC PERS SEVERE, V24, P199, DOI 10.2511/rpsd.24.3.199 ROBSON C, 1991, PROSPECTS PEOPLE LEA, P47 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 Rogers SJ, 2000, J AUTISM DEV DISORD, V30, P399, DOI 10.1023/A:1005543321840 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P169, DOI 10.1017/S0021963098003461 Sainsbury C, 2000, MARTIAN PLAYGROUND U SEGAR M, 1998, COPING ASPERGER SYND Smith M, 2001, POPTRONICS, V2, P25 THOMAS C, 1985, TEACHER TRAINING SPE, P72 WEBSTER A, 2002, ED CHILD PSYCHOL, V19, P54 Wing L, 1996, BRIT MED J, V312, P327 NR 53 TC 4 Z9 4 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD SEP PY 2006 VL 32 IS 5 BP 543 EP 552 DI 10.1111/j.1365-2214.2006.00680.x PG 10 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 071WU UT WOS:000239635400005 PM 16919133 ER PT J AU McConachie, H Robinson, G AF McConachie, H. Robinson, G. TI What services do young children with autism spectrum disorder receive? SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE autism; key workers; multidisciplinary; service utilization; specialist early years provision AB Background:In recent years, standards of good practice have been set for services to young children with autism spectrum disorders. Methods:Data were analysed on children's use of local services during a 2-year follow-up of families involved in an evaluation of a group course for parents. Data collection began prior to publication of the standards. Results:Families' reported experiences changed over time, but for most did not meet standards suggested: involvement with a multi-agency team of professionals, having someone who acted as a key worker, and the child accessing 15 h per week of specialist provision. Conclusion:The development of flexible and responsive services appears to have a long way to go to meet standards set in the Autistic Spectrum Disorders Good Practice Guidance (2002) and the National Autism Plan for Children (2003). C1 Univ Newcastle Upon Tyne, Sch Clin Med Sci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. Univ Newcastle Upon Tyne, Dept Clin Psychol, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. RP McConachie, H (reprint author), Royal Victoria Infirm, Sir James Spence Inst, Sch Clin Med, Queen Vic Rd, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England. EM h.r.mcconachie@ncl.ac.uk CR *AUS COMM, 2003, SERV DIS CHILDR Beresford BA, 1995, EXPERT OPINIONS NATL Bromley J, 2004, AUTISM, V8, P409, DOI 10.1177/1362361304047224 CHRISTIE P, 2005, NAT AUT SOC INT C LO *DFES DOH, 2002, AUT SPECTR DIS GOOD McConachie HR, 1999, CHILD CARE HLTH DEV, V25, P157, DOI 10.1046/j.1365-2214.1999.25220121.x McConachie H, 2005, J PEDIATR-US, V147, P335, DOI 10.1016/j.jpeds.2005.03.056 Milner J, 1996, ARCH DIS CHILD, V75, P399 *NAT AUT SOC ROYAL, 2003, NAT AUT PLAN CHILDR PRATT L, 2005, NAT AUT SOC INT C LO Sussman F., 1999, MORE WORDS HELPING P NR 11 TC 9 Z9 9 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD SEP PY 2006 VL 32 IS 5 BP 553 EP 557 DI 10.1111/j.1365-2214.2006.00672.x PG 5 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 071WU UT WOS:000239635400006 PM 16919134 ER PT J AU Preece, PM Mott, J AF Preece, P. M. Mott, J. TI Multidisciplinary assessment at a child development centre: do we conform to recommended standards? SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE children; neurodisability; multidisciplinary assessment; service delivery AB Background:A proposed standard for the multidisciplinary assessment (MDA) of children with autism has been recently published by the National Autistic Society. This prompted a review of current practice at the child development centre in our local centre, to judge whether we were able to conform to the proposed national standard. The recommendation is that a child should complete a three-stage assessment process from referral to completion of assessment within 30 weeks, with set times for completion of each stage (6, 7 and 17 weeks respectively). We applied this assessment model to children with a range of neurodevelopment problems, as the process of MDA is the same, irrespective of diagnosis. Methods:A retrospective analysis of medical and therapy records of all MDAs was carried out between April 2001 and March 2002. Results:In the 12-month period studied, 52 MDAs were performed. Delays occurred, as judged by the standard, at all three stages of the assessment process. A total of 42% of children were seen within 6 weeks of initial referral, 37% within a further 7 weeks for specialist assessment, and 37% within a further 17 weeks for completion of MDA. As delays occurred at all stages, the cumulative total showed that only 19% of children completed all three stages within the recommended 30-week standard. Barriers encountered included waiting times to see professionals, parental non-attendance and prolonged assessment of complex problems. Some of these factors are outside our control, and on removing these factors the data were re-analysed. This resulted in a slight improvement to 45%, 48% and 49% for completion of stages 1, 2 and 3 respectively. The major reason for delay remained the service capacity. Conclusions:In our experience the standards proposed by the National Autistic Society are not practical within present resources. We suggest that a reasonable expectation is to complete all assessments, from first concern to completed MDA, should be carried out within 52 weeks with present levels of resources. Any further improvement will require additional resources to reduce waiting times and increase the capacity. C1 Chesterfield Royal Hosp NHS Fdn Trust, Calow Chesterfield S44 5BL, England. RP Preece, PM (reprint author), Chesterfield Royal Hosp NHS Fdn Trust, Calow Chesterfield S44 5BL, England. EM philip.preece@chesterfieldroyal.nhs.uk CR *DEP ED SKILLS DEP, 2003, TOG START PRACT GUID *DEP HLTH, 2005, DEP HLTH GUID SERV P Department of Health, 2004, NAT SERV FRAM CHILDR *NAT AUT SOC BEH N, 2003, NAT AUT PLAN CHILDR NR 4 TC 7 Z9 7 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD SEP PY 2006 VL 32 IS 5 BP 559 EP 563 DI 10.1111/j.1365-2214.2006.00656.x PG 5 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 071WU UT WOS:000239635400007 PM 16919135 ER PT J AU Margetts, JK Le Couteur, A Croom, S AF Margetts, J. K. Le Couteur, A. Croom, S. TI Families in a state of flux: the experience of grandparents in autism spectrum disorder SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE autism; child disability; child psychiatry; family functioning; mental health; pervasive developmental disorders ID CHILDREN; SUPPORT; DISABILITIES; CAREGIVERS AB Background:The experience of being a grandparent of a grandchild with autism spectrum disorder (ASD) is a previously under-researched area. This study sets out to examine the grandparents' own perspective in an exploratory way using a qualitative approach to answer the question, 'What is the experience like?' Method:A qualitative research project, using a purposive sampling technique and semi-structured interviews to examine the experiences of six grandparents of children with ASD diagnosed by a specialist team in a second opinion Tier 4 Child and Adolescent Mental Health Service. Results:The experiences of the grandparents were characterized by three Key Themes which emerged from the interviews: (1) The Parental Bond (protective bonding towards grandchild and adult child); (2) Striving for Answers (searching for meaning); (3) Keeping Intact (holding the family together). Conclusion:The study suggests some interesting insights and confirms the need for more attention to this area. A key question raised by the study is how a child-focused multidisciplinary team can embrace its role in delivering a family-centred service. The clinical implications of this project have led to a change of practice in the specialist team. Further research would be appropriate to investigate the therapeutic effectiveness and cost effectiveness of involving grandparents as part of the assessment process. C1 Univ Newcastle Upon Tyne, Sir James Spence Inst, Royal Victoria Infirm, Newcastle Upon Tyne NE1 4HP, Tyne & Wear, England. Northumberland & Tyne & Wear NHS Trust, Newcastle Upon Tyne NE1 4HP, Tyne & Wear, England. Northumbria Univ, Newcastle Upon Tyne NE1 4HP, Tyne & Wear, England. RP Le Couteur, A (reprint author), Univ Newcastle Upon Tyne, Sir James Spence Inst, Royal Victoria Infirm, Queen Vic Rd, Newcastle Upon Tyne NE1 4HP, Tyne & Wear, England. EM a.s.lecouteur@newcastle.ac.uk CR Bowling A., 1997, RES METHODS HLTH INV Department of Health, 2004, NAT SERV FRAM CHILDR Department of Health, 2004, NAT SERV FRAM MENT H Findler LS, 2000, FAM SOC-J CONTEMP H, V81, P370 Garwick AW, 1998, ARCH PEDIAT ADOL MED, V152, P440 Grbich C, 1999, QUALITATIVE RES HLTH Green SE, 2001, INT J AGING HUM DEV, V53, P11, DOI 10.2190/Q7M2-LE06-JLDL-GNWF Hastings RP, 2002, J APPL RES INTELLECT, V15, P97, DOI 10.1046/j.1360 2322.2001.00097.x Hastings RP, 2001, J AUTISM DEV DISORD, V31, P327, DOI 10.1023/A:1010799320795 Heller T., 2000, J GERONTOLOGICAL SOC, V33, P23 Jarbrink K, 2003, J AUTISM DEV DISORD, V33, P395, DOI 10.1023/A:1025058711465 McCallion P, 2004, AM J MENT RETARD, V109, P352, DOI 10.1352/0895-8017(2004)109<352:CEOSGF>2.0.CO;2 Midence K., 1999, AUTISM, V3, P273, DOI [10.1177/1362361399003003005, DOI 10.1177/1362361399003003005] Mirfin-Veitch B., 1996, NZ J DISABILITY STUD, V2, P136 MirfinVeitch B, 1997, FAM RELAT, V46, P305, DOI 10.2307/585129 *NAT AUT SOC, 2005, IMP AUT FAM OBRIEN G, 2003, FORWARD NATL AUTISM, P5 Thomas D, 2003, QUALITATIVE DATA ANA NR 18 TC 13 Z9 14 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD SEP PY 2006 VL 32 IS 5 BP 565 EP 574 DI 10.1111/j.1365-2214.2006.00671.x PG 10 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 071WU UT WOS:000239635400008 PM 16919136 ER PT J AU Santosh, PJ Baird, G Pityaratstian, N Tavare, E Gringras, P AF Santosh, P. J. Baird, G. Pityaratstian, N. Tavare, E. Gringras, P. TI Impact of comorbid autism spectrum disorders on stimulant response in children with attention deficit hyperactivity disorder: a retrospective and prospective effectiveness study SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE ADHD; autism; stimulant medication ID PERVASIVE DEVELOPMENTAL DISORDERS; COMMUNICATION-CHECKLIST; METHYLPHENIDATE AB Background: In the recent past, psychiatrists and paediatricians have avoided prescribing stimulant medication, such as methylphenidate and dexamphetamine to patients with autism spectrum disorders (ASD) because of both doubts about efficacy and concern that these medications make stereotypies worse. Recently, a number of small trials have suggested that methyphenidate does have a role in the management of hyperactivity in children with autistic spectrum disorders. Methods: Children with ASD and attention deficit hyperactivity disorder (ADHD), and children with ADHD without ASD received standard treatment with methyphenidate from one specialist centre. A combination of standardized and novel outcome tools was used to allow both an exploratory retrospective study of 174 children and then a prospective study of a further 52 children to be carried out. Results: After treatment with stimulants, the subjects in both groups showed statistically significant improvements in target symptoms of 'hyperactivity', 'impulsivity', 'inattention', 'oppositionality', 'aggression' and 'intermittent explosive rage'. The Clinical Global Impression-Improvement and efficacy index measures also improved in each group. In both the retrospective and the prospective studies, there was no statistically significant difference in the degree of improvements between each group. Importantly, neither tics nor repetitive behaviours worsened in either group. Children in the 'ADHD-only' group who were prescribed stimulants experienced significant 'nausea', 'giddiness', 'headaches' and 'sleep difficulties', whereas sleep difficulties were the only side effect that emerged in children in the ASD with ADHD group. Conclusions: Both studies presented here support previous findings from smaller studies that show children with autism and ADHD can respond as well to stimulants as children with ADHD alone. Although randomized controlled trials remain the gold standard for efficacy studies, systems like this that allow clinicians to continue rigorous and consistent monitoring for many years have a valuable role to play. Furthermore, such monitoring systems which now exist electronically can easily accumulate large data sets and reveal details about long-term effectiveness and long-term side effects of medication that are unlikely to be discovered in short-term trials. C1 St Thomas Hosp, Elevina Childrens Hosp, London SE1 7EH, England. St Thomas Hosp, Dept Psychol Med, London SE1 7EH, England. RP Gringras, P (reprint author), St Thomas Hosp, Elevina Childrens Hosp, Lambeth Palace Rd, London SE1 7EH, England. 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PD SEP PY 2006 VL 32 IS 5 BP 575 EP 583 DI 10.1111/j.1365-2214.2006.00631.x PG 9 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 071WU UT WOS:000239635400009 PM 16919137 ER PT J AU Gringras, P Santosh, P Baird, G AF Gringras, P. Santosh, P. Baird, G. TI Development of an Internet-based real-time system for monitoring pharmacological interventions in children with neurodevelopmental and neuropsychiatric disorders SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE attention deficit hyperactivity disorder; autism; behaviour; quality of life; quantitative research methods ID QUALITY-OF-LIFE; ADOLESCENTS; INTERVIEW AB Few children have a 'pure' diagnosis of neuropsychiatric disorders such as attention deficit hyperactivity disorder or autism. Most have complex, overlapping symptoms, and it is often these associated and common comorbidities that cause as much, if not more impairments, than the core symptoms. Prescribing decisions are therefore complex and made on the basis of eliciting a range of agreed 'target symptoms'. At present, however, there are no agreed systems that allow monitoring of all areas of potential change, and few services are able to monitor symptoms, side effects, impact on family life and individual children's quality of life systematically. At best many clinics use a plethora of paper-based standardized questionnaires, based on individual diagnoses. This article describes the development of a novel biomedical informatics system that has been designed to allow parents, professionals and children to use a web-based, real-time symptom monitoring system to enable more effective treatments, better pathways of shared care, and more equitable and efficient service delivery for this group of vulnerable children. C1 St Thomas Hosp, Evelina Childrens Hosp, London SE1 7EH, England. Inst Child Hlth, Dept Psychol Med, London, England. Guys Hosp, Newcomen Ctr, London SE1 9RT, England. RP Gringras, P (reprint author), St Thomas Hosp, Evelina Childrens Hosp, Lambeth Palace Rd, London SE1 7EH, England. 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TI Gyrus volume differences in children with Asperger's disorder, high-functioning autism, and bipolar disorder SO CLINICAL NEUROPSYCHOLOGIST LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1385-4046 J9 CLIN NEUROPSYCHOL JI Clin. Neuropsychol. PD SEP PY 2006 VL 20 IS 3 BP 583 EP 583 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA 071MT UT WOS:000239607000046 ER PT J AU Fisher, SE AF Fisher, Simon E. TI Tangled webs: Tracing the connections between genes and cognition SO COGNITION LA English DT Review DE genetics; linkage analysis; association analysis; developmental dyslexia; speech and language disorders; autism; FOXP2 ID QUANTITATIVE-TRAIT LOCUS; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY DISORDER; DYSLEXIA SUSCEPTIBILITY LOCUS; CHROMOSOME 6P INFLUENCES; DEVELOPMENTAL DYSLEXIA; LANGUAGE DISORDER; READING-DISABILITY; GENOMEWIDE SCAN; COMPLEX TRAITS AB The rise of molecular genetics is having a pervasive influence in a wide variety of fields, including research into neurodevelopmental disorders like dyslexia, speech and language impairments, and autism. There are many studies underway which are attempting to determine the roles of genetic factors in the aetiology of these disorders. Beyond the obvious implications for diagnosis, treatment and understanding, success in these efforts promises to shed light on the links between genes and aspects of cognition and behaviour. However, the deceptive simplicity of finding correlations between genetic and phenotypic variation has led to a common misconception that there exist straightforward linear relationships between specific genes and particular behavioural and/or cognitive outputs. The problem is exacerbated by the adoption of an abstract view of the nature of the gene, without consideration of molecular, developmental or ontogenetic frameworks. To illustrate the limitations of this perspective, I select two cases from recent research into the genetic underpinnings of neurodevelopmental disorders. First, I discuss the proposal that dyslexia can be dissected into distinct components specified by different genes. Second, I review the story of the FOXP2 gene and its role in human speech and language. In both cases, adoption of an abstract concept of the gene can lead to erroneous conclusions, which are incompatible with current knowledge of molecular and developmental systems. Genes do not specify behaviours or cognitive processes; they make regulatory factors, signalling molecules, receptors, enzymes, and so on, that interact in highly complex networks, modulated by environmental influences, in order to build and maintain the brain. I propose that it is necessary for us to fully embrace the complexity of biological systems, if we are ever to untangle the webs that link genes to cognition. (c) 2006 Elsevier B.V. All rights reserved. C1 Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. RP Fisher, SE (reprint author), Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England. 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As a computer-based medium, Virtual Environments (VEs) offer a potentially useful tool for social skills training for people with autistic spectrum disorders (ASDs). However, there are some concerns over whether people with ASDs can understand, use and interpret the technology appropriately. This paper adopts a qualitative case-study approach to report observations of, and comments from, two adolescent boys with ASDs, gathered during a series of sessions using a virtual cafe and bus environment. Although there were signs of repetitive behaviours, literal interpretation of the scenes, and that the VEs were treated as not having real-world relevance, these were not the dominant modes of responding. Instead, participants seemed to interpret the scenes meaningfully and appreciated the opportunities to discuss appropriate social responses with a facilitator sitting alongside. They enjoyed using the VEs and provided specific examples of how the VEs had helped, or could help, them in the real world. This gives encouraging support for the idea that VEs can be used and interpreted meaningfully by at least some students with ASDs. The paper concludes with some considerations for the future development of VEs for members of this population. (c) 2004 Elsevier Ltd. All rights reserved. C1 Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Parsons, S (reprint author), Univ Birmingham, Sch Educ, Birmingham B15 2TT, W Midlands, England. 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PD SEP PY 2006 VL 47 IS 2 BP 186 EP 206 DI 10.1016/j.compedu.2004.10.003 PG 21 WC Computer Science, Interdisciplinary Applications; Education & Educational Research SC Computer Science; Education & Educational Research GA 062EY UT WOS:000238928600004 ER PT J AU Riikonen, R Makkonen, I Vanhala, R Turpeinen, U Kuikka, J Kokki, H AF Riikonen, Raili Makkonen, Ismo Vanhala, Raija Turpeinen, Ursula Kuikka, Jyrki Kokki, Hannu TI Cerebrospinal fluid insulin-like growth factors IGF-1 and IGF-2 in infantile autism SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID FACTOR-I; BRAIN SIZE; RAT-BRAIN; CHILDREN; EXPRESSION; DISORDER; PATHWAYS; SURVIVAL; SYSTEM; MRI AB There has been little exploration of major biologic regulators of cerebral development in autism. We measured insulin-like growth factors (IGF) -1 and -2 from cerebrospinal fluid (CSF) by radio immunoassay in 25 children with autism (median age 5y 5mo; range 1y 11mo-15y 10mo; 20 males, 5 females), and in 16 age-matched comparison children without disability (median age 7y 4mo; range 1y 1mo-15y 2mo; eight males, eight females). IGF-1 and -2 concentrations were further correlated with age of patients and head size. OF IGF-1 concentration was significantly lower in patients with autism than in the comparison group. The CSF concentrations of children with autism under 5 years of age were significantly lower than their age-matched comparisons. The head circumferences correlated with CSF IGF-1 in children with autism but no such correlation was found in the comparison group. There was no difference between the two groups in CSF IGF-2 concentrations. No patients with autism had macrocephaly. We conclude that low concentrations of CSF IGF-1 at an early age might be linked with the pathogenesis in autism because IGF-1 is important for the survival of Purkinje cells of the cerebellum. The head growth might be explained by the actions of IGF-1 and -2 reflected in CSF concentrations. C1 Univ Kuopio, Cent Hosp, Dept Child Neurol, FI-70211 Kuopio, Finland. Hosp Children & Adolescents, Dept Clin Neurol, Helsinki, Finland. Univ Helsinki, Cent Hosp, Helsinki, Finland. Univ Kuopio, Cent Hosp, Dept Anaesthesiol & Intens Care, FI-70211 Kuopio, Finland. RP Riikonen, R (reprint author), Univ Kuopio, Cent Hosp, Dept Child Neurol, POB 1627, FI-70211 Kuopio, Finland. 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Med. Child Neurol. PD SEP PY 2006 VL 48 IS 9 BP 751 EP 755 DI 10.1017/S0012162206001605 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 079KA UT WOS:000240173500011 PM 16904022 ER PT J AU Losh, M Capps, L AF Losh, Molly Capps, Lisa TI Understanding of emotional experience in autism: Insights from the personal accounts of high-functioning children with autism SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article DE autism; Asperger's syndrome; emotion; language ID INDIVIDUAL-DIFFERENCES; SELF; RECOGNITION; COMPETENCE; PERCEPTION; COGNITION; DISORDER; MEMORY; ADULTS; MIND AB In this study, the authors investigate emotional understanding in autism through a discourse analytic framework to provide a window into children's strategies for interpreting emotional versus nonemotional encounters and consider the implications for the mechanisms underlying emotional understanding in typical development. Accounts were analyzed for thematic content and discourse structure. Whereas high-functioning children with autism were able to discuss contextually appropriate accounts of simple emotions, their strategies for interpreting all types of emotional (but not nonemotional) experiences differed from those used by typically developing children. High-functioning children with autism were less inclined to organize their emotional accounts in personalized causal-explanatory frameworks and displayed a tendency to describe visually salient elements of experiences seldom observed among comparison children. Findings suggest that children with autism possess less coherent representations of emotional experiences and use alternative strategies for interpreting emotionally evocative encounters. Discussion focuses on the significance of these findings for informing the nature of emotional dysfunction in autism as well as implications for theories of emotional understanding in typical development. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA. RP Losh, M (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, CB 3366, Chapel Hill, NC 27599 USA. EM losh@med.unc.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Attwood T., 1998, ASPERGERS SYNDROME G Baron-Cohen S, 2001, INT REV RES MENT RET, V23, P169 Barrett K. C., 1987, HDB INFANT DEV, P555 Bettelheim B., 1967, EMPTY FORTRESS INFAN Bowler DM, 2000, J AUTISM DEV DISORD, V30, P295, DOI 10.1023/A:1005575216176 Bruner J, 1986, ACTUAL MINDS POSSIBL Bruner J. 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PD SEP PY 2006 VL 42 IS 5 BP 809 EP 818 DI 10.1037/0012-1649.42.5.809 PG 10 WC Psychology, Developmental SC Psychology GA 084JZ UT WOS:000240530500005 PM 16953688 ER PT J AU Mancil, GR AF Mancil, G. Richmond TI Functional communication training: A review of the literature related to children with autism SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Review ID BEHAVIOR PROBLEMS; DISABILITIES AB Numerous researchers have employed functional communication training (FCT) to address both the communication and behavioral needs of children with autism. Thus, the purpose of this review is to examine FCT, particularly, the environments and individuals involved in the training and the effectiveness of FCT with children who have a diagnosis of Autism Spectrum Disorder (ASD) and to provide suggestions for practitioners and researchers. FCT consistently reduces challenging behavior and increases communication; however, the majority of research is clinically based and focuses on one communication and. Future research teams should address maintenance and generalization by training teachers in classrooms and parents in homes while collecting data across time. C1 Univ Florida, Dept Special Educ, Gainesville, FL 32611 USA. RP Mancil, GR (reprint author), Univ Florida, Dept Special Educ, G-315 Norman Hall,POB 117050, Gainesville, FL 32611 USA. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bott C, 1997, J INTELL DISABIL RES, V41, P3, DOI 10.1111/j.1365-2788.1997.tb00671.x Brady N. C., 1997, FOCUS AUTISM OTHER D, V12, P95 CARR EG, 1985, J APPL BEHAV ANAL, V18, P111, DOI 10.1901/jaba.1985.18-111 CHUNG MC, 1995, EUR J PSYCHIAT, V9, P83 DUNLAP G, 2005, WHAT WORKS BRIEF Durand V. 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Woods-Groves, Suzanne Williams, Thomas O., Jr. Fall, Anna-Maria TI Reliability and validity of the Pervasive Developmental Disorders Rating Scale and the Gilliam Autism Rating Scale SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID BEHAVIOR AB The psychometric properties of the Pervasive Developmental Disorders Rating scale (Eaves, 2003) and the Gilliam Autism Rating Scale (Gilliam, 1995) were investigated in this study. One hundred thirty-four individuals with autism, other pervasive developmental disorders, or conditions frequently confused with autism participated in the study. The results indicated that, with one exception, the reliability of the scores from both instruments met or exceeded standards for use in screening decisions. The reliability of the total scores from both instruments exceeded .90. Validity coefficients computed between the two sets of scores indicated that the instruments measured similar constructs (e.g., (rpddrs total x gars total) = .84). The scores from both instruments discriminated between children with autism and children who were not autistic to a statistically significant degree. C1 Auburn Univ, Dept Rehabil & Special Educ, Auburn, AL 36849 USA. Virginia Polytech Inst & State Univ, Blacksburg, VA 24061 USA. RP Eaves, RC (reprint author), Auburn Univ, Dept Rehabil & Special Educ, 1228 Haley Ctr, Auburn, AL 36849 USA. 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PD SEP PY 2006 VL 41 IS 3 BP 300 EP 309 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 075VB UT WOS:000239912300009 ER PT J AU Waterhouse, L AF Waterhouse, Lynn TI Inadequate evidence for multiple intelligences, Mozart effect, and emotional intelligence theories SO EDUCATIONAL PSYCHOLOGIST LA English DT Article ID MISSING COGNITIVE MATTER; PERSONALITY; PERFORMANCE; MUSIC; OXYTOCIN; INSTRUCTION; AUTISM; LIFE; PERSPECTIVE; ABILITIES AB I (Waterhouse, 2006) argued that, because multiple intelligences, the Mozart effect, and emotional intelligence theories have inadequate empirical support and are not consistent with cognitive neuroscience findings, these theories should not be applied in education. Proponents countered that their theories had sufficient empirical support, were consistent with cognitive neuroscience findings, and should be applied in education (Cherniss, Extein, Goleman, & Weissberg, 2006; Gardner & Moran, 2006; Rauscher & Hinton, 2006). However, Gardner and Moran offered no validating evidence for multiple intelligences, Rauscher and Hinton concluded that "listening-to-Mozart" studies should be disregarded, and Cherniss, Extein, Goleman, and Weissberg agreed that emotional intelligence lacked a unitary empirically supported construct. My reply addresses theory proponents' specific criticisms of my review and reasserts my original claims. C1 Coll New Jersey, Ewing, NJ 08628 USA. RP Waterhouse, L (reprint author), Coll New Jersey, 234 Bliss Hall, Ewing, NJ 08628 USA. 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Psychol. PD FAL PY 2006 VL 41 IS 4 BP 247 EP 255 DI 10.1207/s15326985ep4104_5 PG 9 WC Education & Educational Research; Psychology, Educational SC Education & Educational Research; Psychology GA 108HI UT WOS:000242230500005 ER PT J AU Windham, GC Zhang, LX Gunier, R Croen, LA Grether, JK AF Windham, Gayle C. Zhang, Lixia Gunier, Robert Croen, Lisa A. Grether, Judith K. TI Autism spectrum disorders in relation to distribution of hazardous air pollutants in the San Francisco Bay area SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE air toxics; autism; autism spectrum disorders; diesel; mercury; metals; neurodevelopment; neurotoxicants; solvents; vinyl chloride ID MATERNAL OCCUPATIONAL-EXPOSURE; PUBLIC-HEALTH IMPLICATIONS; MERCURY-VAPOR EXPOSURE; TOXICS CONCENTRATIONS; ENVIRONMENTAL-FACTORS; PERSONAL EXPOSURE; PRENATAL EXPOSURE; UNITED-STATES; CALIFORNIA; CHILDREN AB OBJECTIVE: To explore possible associations between autism spectrum disorders (ASD) and environmental exposures, we linked the California autism surveillance system to estimated hazardous air pollutant (HAP) concentrations compiled by the U.S. Environmental Protection Agency. METHODS: Subjects included 284 children with ASD and 657 controls, born in 1994 in the San Francisco Bay area. We assigned exposure level by census tract of birth residence for 19 chemicals we identified as potential neurotoxicants, developmental toxicants, and/or endocrine disruptors from the 1996 HAPs database. Because concentrations of many of these were highly correlated, we combined the chemicals into mechanistic and structural groups, calculating summary index scores. We calculated ASD risk in the upper quartiles of these group scores or individual chemical concentrations compared with below the median, adjusting for demographic factors. RESULTS: The adjusted odds ratios (AORs) were elevated by 50% in the top quartile of chlorinated solvents and heavy metals [95% confidence intervals (CIs), 1.1-2.1], but not for aromatic solvents. Adjusting for these three groups simultaneously led to decreased risks for the solvents and increased risk for metals (AORs for metals: fourth quartile = 1.7; 95% Cl, 1.0-3.0; third quartile = 1.95; 95% CI, 1.2-3.1). The individual compounds that contributed most to these associations included mercury, cadmium, nickel, trichloroethylene, and vinyl chloride. CONCLUSIONS: Our results suggest a potential association between autism and estimated metal concentrations, and possibly solvents, in ambient air around the birth residence, requiring confirmation and more refined exposure assessment in future studies. C1 Calif Dept Hlth Serv, Div Environm & Occupat Dis Control, Richmond, CA 94804 USA. Impace Assessment Inc, La Jolla, CA USA. Kaiser Permanente Med Care Program, Div Res, Oakland, CA 94611 USA. RP Windham, GC (reprint author), Calif Dept Hlth Serv, Div Environm & Occupat Dis Control, 850 Marina Bay Pkwy,Bldg P, Richmond, CA 94804 USA. 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PD SEP PY 2006 VL 114 IS 9 BP 1438 EP 1444 DI 10.1289/ehp.9120 PG 7 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 087PZ UT WOS:000240755700045 PM 16966102 ER PT J AU Desombre, H Malvy, J Roux, S de Villard, R Sauvage, D Dalery, J Lenoir, P AF Desombre, Hugues Malvy, Joelle Roux, Sylvie de Villard, Regis Sauvage, Dominique Dalery, Jean Lenoir, Pascal TI Autism and developmental delay - A comparative clinical study in very young children using IBSE scale SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; developmental delay; early features; pre-school children ID FAMILY HOME MOVIES; RETROSPECTIVE VIDEO ANALYSIS; SPECTRUM DISORDERS; MENTAL DISABILITY; EARLY RECOGNITION; EARLY SYMPTOMS; AGE; INFANTS; LIFE; RETARDATION AB This study improves the knowledge of early autistic symptomatology and research concerning (i) the significant differences in the behaviors of children with autistic disorder (AD) and children with a developmental delay (DD), and (ii) the influence of the cognitive delay on symptomatology. Two groups of 20 young children (7-42 months) were compared: children with AD, and those with DD. The groups were paired by chronological and developmental age. The comparison was extended to four subgroups composed according to age (younger and older children-< 24 months, > 24 months) and to the global development quotient (GDQ) (the more and less delayed). Each child was evaluated with the Infant Behavior Summarized Evaluation scale (IBSE). For the younger AD children, significant differences affected social communication and their adaptation to the environment (intolerance to frustration, resistance to change). For the older children (> 24 months), this study showed the rapid progression of the number of distinctive signs between AD and DD children according to age and/or developmental level. Cognitive delay has an important influence on the symptomatology at the moment of initial recognition of an autistic syndrome. This study is a complement for the fuller understanding of the nature and early diagnosis of disorders specific to autism at the earliest phases of development. C1 Hop Edouard Herriot, Dept Pediat, Unite Psychopathol Enfant & Adolescent, F-69437 Lyon 03, France. Univ Lyon 1, CHS Vinatier, Equipe Accueil 3092, Bron, France. Ctr Hosp Reg & Univ, Serv Univ Pedopsychiat, Hop Bretonneau, Tours, France. Ctr Hosp Reg & Univ, Serv Univ Explorat Fonct & Neurophysiol Pedopsych, Hop Bretonneau, Tours, France. RP Desombre, H (reprint author), Hop Edouard Herriot, Dept Pediat, Unite Psychopathol Enfant & Adolescent, Pl Arsonval, F-69437 Lyon 03, France. 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Child Adolesc. Psych. PD SEP PY 2006 VL 15 IS 6 BP 343 EP 351 DI 10.1007/s00787-006-0540-9 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 078AC UT WOS:000240072200005 PM 16614787 ER PT J AU Anagnostou, E Chaplin, W Rusoff, J Soorya, L Hollander, E AF Anagnostou, E. Chaplin, W. Rusoff, J. Soorya, L. Hollander, E. TI Divalproex sodium for the treatment of irritability in autism SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 19th Congress of the European-College-of-Neuropsychopharmacology CY SEP 16-20, 2006 CL Paris, FRANCE SP European Coll Neuropsychopharmacol C1 Mt Sinai Sch Med, New York, NY USA. CR ANAGNOSTOU E, 2006, IN PRESS J CLIN PSYC Hollander E, 2005, BIOL PSYCHIAT, V58, P226, DOI 10.1016/j.biopsych.2005.03.040 HOLLANDER E, 2005, INT J NEUROPSYCHOPH, V15, P1 NR 3 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD SEP PY 2006 VL 16 SU 4 BP S524 EP S524 DI 10.1016/S0924-977X(06)70724-6 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 087VQ UT WOS:000240771302131 ER PT J AU Anagnostou, E Fan, J Hollander, E AF Anagnostou, E. Fan, J. Hollander, E. TI Functional MRI of response inhibition in autism SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 19th Congress of the European-College-of-Neuropsychopharmacology CY SEP 16-20, 2006 CL Paris, FRANCE SP European Coll Neuropsychopharmacol C1 CUNY Mt Sinai Sch Med, New York, NY 10029 USA. CR ANAGNOSTOU E, 2006, IN PRESS J CLIN PSYC Hollander E, 2005, BIOL PSYCHIAT, V58, P226, DOI 10.1016/j.biopsych.2005.03.040 HOLLANDER E, 2005, INT J NEUROPSYCHOPH, V15, P1 NR 3 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD SEP PY 2006 VL 16 SU 4 BP S531 EP S532 DI 10.1016/S0924-977X(06)70737-4 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 087VQ UT WOS:000240771302144 ER PT J AU Jeon, JWJ Chung, SHC Hong, JPH Yoo, HIY AF Jeon, J. W. J. Chung, S. H. C. Hong, J. P. H. Yoo, H. I. Y. TI Association of DAO and DAOA genes with autism spectrum disorders in Korean boys SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 19th Congress of the European-College-of-Neuropsychopharmacology CY SEP 16-20, 2006 CL Paris, FRANCE SP European Coll Neuropsychopharmacol ID SCHIZOPHRENIA C1 Asan Med Ctr, Dept Psychiat, Seoul, South Korea. CR BAILLY C, 1995, MED MALADIES INFECT, V25, P1 Chumakov I, 2002, P NATL ACAD SCI USA, V99, P13675, DOI 10.1073/pnas.182412499 Collier DA, 2003, EUR J PHARMACOL, V480, P177, DOI 10.1016/j.ephar.2003.08.105 NR 3 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD SEP PY 2006 VL 16 SU 4 BP S526 EP S526 DI 10.1016/S0924-977X(06)70727-1 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 087VQ UT WOS:000240771302134 ER PT J AU Staal, W Franke, L Vorstman, JAS Hochstenbach, R Van Engeland, H AF Staal, W. Franke, L. Vorstman, J. A. S. Hochstenbach, R. Van Engeland, H. TI Autism candidate genes in cytogenetic regions of interest identified with a gene interaction network SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 19th Congress of the European-College-of-Neuropsychopharmacology CY SEP 16-20, 2006 CL Paris, FRANCE SP European Coll Neuropsychopharmacol C1 Rudolf Magnus Inst Neurosci, Dept Child & Adolescent Psychiat, NL-3508 TA Utrecht, Netherlands. Univ Utrecht, Utrecht, Netherlands. CR STAAL WG, 2006, MOL PSYCH JAN NR 1 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD SEP PY 2006 VL 16 SU 4 BP S176 EP S176 DI 10.1016/S0924-977X(06)70048-7 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 087VQ UT WOS:000240771300038 ER PT J AU Williams, TI AF Williams, Tim I. TI Evaluating effects of aromatherapy massage on sleep in children with autism: A pilot study SO EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE LA English DT Article DE aromatherapy; massage; autism; sleep; children ID DEMENTIA AB Previous studies have found beneficial effects of aromatherapy massage for agitation in people with dementia, for pain relief and for poor sleep. Children with autism often have sleep difficulties, and it was thought that aromatherapy massage might enable more rapid sleep onset, less sleep disruption and longer sleep duration. Twelve children with autism and learning difficulties (2 girls and 10 boys aged between 12 years 2 months to 15 years 7 months) in a residential school participated in a within subjects repeated measures design: 3 nights when the children were given aromatherapy massage with lavender oil were compared with 14 nights when it was not given. The children were checked every 30 min throughout the night to determine the time taken for the children to settle to sleep, the number of awakenings and the sleep duration. One boy's data were not analyzed owing to lengthy absence. Repeated measures analysis revealed no differences in any of the sleep measures between the nights when the children were given aromatherapy massage and nights when the children were not given aromatherapy massage. The results suggest that the use of aromatherapy massage with lavender oil has no beneficial effect on the sleep patterns of children with autism attending a residential school. It is possible that there are greater effects in the home environment or with longer-term interventions. C1 Berkshire Healthcare NHS Trust, Dept Psychol, Reading RG1 5LF, Berks, England. Univ Reading, Sch Psychol, Reading RG6 2AH, Berks, England. RP Williams, TI (reprint author), Berkshire Healthcare NHS Trust, Dept Psychol, 3-5 Craven Rd, Reading RG1 5LF, Berks, England. 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Med. PD SEP PY 2006 VL 3 IS 3 BP 373 EP 377 DI 10.1093/ecam/nel017 PG 5 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 079TB UT WOS:000240199700011 PM 16951722 ER PT J AU Schaefer, GB Lutz, RE AF Schaefer, G. Bradley Lutz, Richard E. TI Diagnostic yield in the clinical genetic evaluation of autism spectrum disorders SO GENETICS IN MEDICINE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; FRAGILE-X-SYNDROME; INFANTILE-AUTISM; DELETION SYNDROME; MENTAL-RETARDATION; ADENYLOSUCCINATE LYASE; ANGELMAN-SYNDROME; ETIOLOGIC YIELD; MECP2 MUTATIONS; RETT-SYNDROME AB Purpose: Clinical geneticists are often asked to evaluate patients with autism spectrum disorders (ASDs) in reference to questions about cause and recurrence risk. Recent advances in diagnostic testing technology have greatly increased the options available to them. It is not currently clear what the overall diagnostic yield of a battery of tests, either collectively or individually, might be. The purpose of this study was to evaluate the diagnostic yield of a stepwise approach we have implemented in our clinics. Methods: We used a three-tiered neurogenetic evaluation scheme designed to determine the cause of ASDs in patients referred for clinical genetic consultation. We reviewed the results of our diagnostic evaluations on all patients referred with a confirmed diagnosis of autism over a 3-year period. Results: By using this approach, we found an overall diagnostic yield for ASDs of more than 40%. This represents a significant increase in the diagnostic yield reported just a few years ago. Conclusions: Given the implications of these diagnoses on recurrence risk and associated medical conditions, a targeted neurogenetic evaluation of all persons with ASDs seems warranted. 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PD SEP PY 2006 VL 8 IS 3 BP 325 EP 326 PG 2 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA 076RV UT WOS:000239976300009 ER PT J AU McGuigan, N Nunez, M AF McGuigan, Nicola Nunez, Maria TI Executive functioning by 18-24-month-old children: Effects of inhibition, working memory demands and narrative in a novel detour-reaching task SO INFANT AND CHILD DEVELOPMENT LA English DT Article DE executive function; arbitrary means; causal means; working memory; inhibition; rationale generativity ID A-NOT-B; YOUNG-CHILDREN; PRESCHOOL-CHILDREN; RESPONSE CONTROL; SYMBOLIC PLAY; PERFORMANCE; RECALL; MIND; INFANTS; AUTISM AB Infants can inhibit a prepotent but wrong action towards a goal in order to perform a causal means-action. It is not clear, however, whether infants can perform an arbitrary means-action while inhibiting a prepotent response. In four experiments, we explore this executive functioning in 18-24-month-old children. The working memory and inhibition demands in a novel means-end problem were systematically varied in terms of the type and combination of means-action(s) (causal or arbitrary) contained within the task, the number of means-actions (I or 2), the goal visual availability and whether the task was accompanied by a narrative. Experiments 1 and 2 showed that children performed tasks that contained causal as opposed to arbitrary information more accurately; accuracy was also higher in tasks containing only one step. Experiment 2 also demonstrated that performance in the arbitrary task improved significantly when all sources of prepotency were removed. In Experiment 3, task performance improved when the two means-actions were intelligibly linked to the task goal. 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PD SEP PY 2006 VL 19 IS 3 BP 237 EP 237 PG 1 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 064VK UT WOS:000239117600090 ER PT J AU van den Broek, A AF van den Broek, A. TI What are the social-emotional skills which children with an autism spectrum disorder and intellectual disability are able to learn? SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Meeting Abstract EM a.vd.broek@vizier.nl NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PD SEP PY 2006 VL 19 IS 3 BP 272 EP 272 PG 1 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 064VK UT WOS:000239117600353 ER PT J AU Kraijer, D AF Kraijer, D. TI Identification of autism spectrum disorders: Presentation of the new manual of the PDD-MRS SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Meeting Abstract EM dirk.kraijer@vanboeijen.nl NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PD SEP PY 2006 VL 19 IS 3 BP 274 EP 274 PG 1 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 064VK UT WOS:000239117600365 ER PT J AU Campbell, JM AF Campbell, Jonathan M. TI Changing children's attitudes toward autism: A process of persuasive communication SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; attitudes; persuasion; inclusion; peers ID MENTALLY-RETARDED PEERS; BEHAVIORAL INTENTIONS; EDUCATIONAL INTERVENTION; HANDICAPPED-CHILDREN; SOCIAL-BEHAVIOR; CONTACT THEORY; ILLNESS; DISABILITIES; STIGMA; PERCEPTIONS AB The purposes of this paper are two-fold. First, the initial introduction of a child with autism to typically developing peers is conceptualized as a process of persuasive communication. Second, relevant literature is organized and reviewed according to important components and processes involved in persuasive communication, including effects of source, message, receiver, and channel. Research about perceptions of children with autism is highlighted when available. 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Winton, Alan S. W. Fisher, Barbara C. Wahler, Robert G. McAleavey, Kristen Singh, Judy Sabaawi, Mohamed TI Mindful parenting decreases aggression, noncompliance, and self-injury in children with autism SO JOURNAL OF EMOTIONAL AND BEHAVIORAL DISORDERS LA English DT Article ID MENTAL-RETARDATION; INTERVENTION; DISABILITIES; PRESCHOOL; INDIVIDUALS; MEDITATION; STRESS; BOYS AB Parent-child transactions provide an important social context for the development of adaptive and problem behaviors in young children with autism. Teaching parents to develop alternative transactional pathways often leads to positive behavioral patterns in their children. We taught three parents the philosophy and practice of mindfulness in a 12-week course and assessed the outcome of the training on their children's behavior. In addition, the mothers rated satisfaction with their parenting skills and interactions with their children. Results showed that the mothers' mindful parenting decreased their children's aggression, noncompliance, and self-injury and increased the mothers' satisfaction with their parenting skills and interactions with their children. We speculated on the possible reasons for the efficacy of mindful parenting in decreasing the children's problem behaviors without the application of specific, programmed contingencies for the children's behavior. C1 ONE Res Inst, Chesterfield, VA 23832 USA. RP Singh, NN (reprint author), ONE Res Inst, 7401 Sparkleberry Ln, Chesterfield, VA 23832 USA. CR Baer RA, 2003, CLIN PSYCHOL-SCI PR, V10, P125, DOI 10.1093/clipsy/bpg015 Borthwick-Duffy SA, 1996, QUALITY LIFE, P105 Briesmeister J. M, 1998, HDB PARENT TRAINING CARR EG, 1999, FUNCTIONAL ANAL PROB Curtis WJ, 2003, DEV PSYCHOPATHOL, V15, P773, DOI 10.1017/S0954579403000373 Davidson RJ, 2003, PSYCHOSOM MED, V65, P564, DOI 10.1097/01.PSY.0000077505.67574.E3 Didden R, 1997, AM J MENT RETARD, V101, P387 Eyberg S. 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PD FAL PY 2006 VL 14 IS 3 BP 169 EP 177 DI 10.1177/10634266060140030401 PG 9 WC Education, Special; Psychology, Educational; Psychology, Multidisciplinary SC Education & Educational Research; Psychology GA 076RH UT WOS:000239974900004 ER PT J AU Bonnet, C Gregoire, MJ Brochet, K Raffo, E Leheup, B Jonveaux, P AF Bonnet, C. Gregoire, M. J. Brochet, K. Raffo, E. Leheup, B. Jonveaux, P. TI Pure de-novo 5 Mb duplication at Xp11.22-p11.23 in a male: phenotypic and molecular characterization SO JOURNAL OF HUMAN GENETICS LA English DT Article DE X chromosome; duplication; array-CGH; mental retardation; autism; FTSJ1 gene; PQBP1 gene; HDAC6 gene ID LINKED MENTAL-RETARDATION; RANDOM X-INACTIVATION; BINDING-PROTEIN; HUMAN GENOME; CHROMOSOME; TRANSCRIPTION; MUTATIONS; STATURE; PQBP-1; FTSJ1 AB Males with duplications within the short arm of the X chromosome are rare and most cases are inherited from a maternal heterozygote. Here we describe the first detailed characterization of a de-novo Xp duplication delineated to Xp11.22 -> Xp11.23 in a 15-year-old male with moderate mental impairment, autistic-like behaviour, short stature, and mild dysmorphic features. Chromosome analysis (550 band resolution) was normal and comparative genomic hybridization (CGH) analysis on metaphase spreads detected duplication on Xp11. Further characterization of the duplication by array CGH, FISH experiments with specific BAC probes, and genotyping with microsatellite markers helped to determine proximal and distal breakpoints giving a size of the duplication of approximately 5Mb. As far as we are aware this is the first described male with isolated microduplication on Xp11.22-Xp11.23. Among the genes included within the duplicated region, and particularly those which are outside copy number polymorphisms, we discuss the relationship of FTSJ1, PQBP1 and HDAC6 with the clinical symptoms of our patient. C1 CHU Nancy Brabois, Med Genet Lab, F-54511 Vandoeuvre Les Nancy, France. CHU Nancy, Serv Med Infantile 1, Nancy, France. CHU Nancy, Serv Med Infantile & Genet Clin 3, Nancy, France. RP Jonveaux, P (reprint author), CHU Nancy Brabois, Med Genet Lab, F-54511 Vandoeuvre Les Nancy, France. 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Hum. Genet. PD SEP PY 2006 VL 51 IS 9 BP 815 EP 821 DI 10.1007/s10038-006-0023-3 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 083PC UT WOS:000240469700012 PM 16900295 ER PT J AU Noens, I van Berckelaer-Onnes, I Verpoorten, R Duijn, G AF Noens, I. van Berckelaer-Onnes, I. Verpoorten, R. van Duijn, G. TI The ComFor: an instrument for the indication of augmentative communication in people with autism and intellectual disability SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE augmentative communication; autism; diagnostic instrument; intellectual disability ID LANGUAGE; SENSE AB The ComFor (Forerunners in Communication) is an instrument to explore underlying competence for augmentative communication. More specifically, it measures perception and sense-making of non-transient forms of communication at the levels of presentation and representation. The target group consists primarily of individuals with autism and intellectual disability (ID) without or with only limited verbal communication. The ComFor is suitable for children and adults with a developmental level between 12 and 60 months. This paper describes the theoretical framework and structure of the ComFor, the results of a study on its psychometric properties and its clinical uses. The ComFor was tested on a sample of 623 children and adults from the Netherlands and Flanders: a group with autism and ID (n = 310); a group with ID without autism (n = 174); and a control group of typically developing children (n = 139). The data generally support the reliability and validity of the ComFor. Internal consistency, inter-rater and test-retest reliability were found to be good. Construct validity (internal structure, convergent and divergent patterns) was established in different ways. 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L., 1997, HDB AUTISM PERVASIVE, P539 Stevens J, 1992, APPL MULTIVARIATE ST, V2nd VANBERCKELAERON.IA, 1996, NEDERLANDS TIJDSCHRI, V22, P79 VERPOORTEN R, COMFOR FORERUNNERS C Verpoorten R., 2004, COMVOOR VOORLOPERS C Verpoorten R. A. W., 1996, NEDERLANDS TIJDSCHRI, V22, P106 Wetherby AM, 2000, COMM LANG INTERVEN, V9, P109 *WHO, 1994, INT CLASSIFICATION D WILLEMS J, 1996, COMMUNICATIE PROFIEL WILLEMS JB, 1996, THESIS U BRABANT TIL NR 33 TC 9 Z9 9 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD SEP PY 2006 VL 50 BP 621 EP 632 DI 10.1111/j.1365-2788.2006.00807.x PN 9 PG 12 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 066VJ UT WOS:000239258100001 PM 16901289 ER PT J AU Willatt, L Kenwrick, S Parkin, G Whittaker, J Baralle, D AF Willatt, Lionel Kenwrick, S. Parkin, G. Whittaker, J. Baralle, D. TI A de novo microdeletion of 5p15.1 in a boy with autism spectrum disorder SO JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT British Human Genetics Conference CY SEP 18-20, 2006 CL York, ENGLAND HO Univ York C1 Addenbrookes Hosp, Cambridge Univ Hosp NHS Fdn Trust, Cambridge, England. EM lionel.willatt@addenbrookes.nhs.uk NR 0 TC 0 Z9 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD SEP PY 2006 VL 43 SU 1 BP S95 EP S95 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 090NK UT WOS:000240957800234 ER PT J AU Singer, HS Morris, CM Williams, PN Yoon, DY Hong, JJ Zimmerman, AW AF Singer, Harvey S. Morris, Christina M. Williams, Phillip N. Yoon, Dustin Y. Hong, John J. Zimmerman, Andrew W. TI Antibrain antibodies in children with autism and their unaffected siblings SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE autism; immunoblotting; autoantibodies; siblings; 100 kDa; 73 kDa ID SPECTRUM DISORDERS; CHILDHOOD AUTISM; RISK-FACTORS; BRAIN; SERUM; AUTOANTIBODIES; PROTEINS; BEHAVIOR; GENES AB Serum autoantibodies to human brain, identified by ELISA and Western immunoblotting, were evaluated in 29 children with autism spectrum disorder (22 with autistic disorder), 9 non-autistic siblings and 13 controls. More autistic subjects than controls had bands at 100 kDa in caudate, putamen and prefrontal cortex (p < 0.01) as well as larger peak heights of bands at 73 kDa in the cerebellum and cingulate gyrus. Both autistic disorder subjects and their matched non-autistic siblings had denser bands (peak height and/or area under the curve) at 73 kDa in the cerebellum and cingulate gyrus than did controls (p < 0.01). Results suggest that children with autistic disorder and their siblings exhibit differences compared to controls in autoimmune reactivity to specific epitopes located in distinct brain regions. (c) 2006 Elsevier B.V. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21287 USA. Kennedy Krieger Inst, Baltimore, MD 21287 USA. RP Singer, HS (reprint author), Johns Hopkins Univ Hosp, Div Pediat Neurol, 600 N Wolfe St,Jefferson St Bldg 124, Baltimore, MD 21287 USA. 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Neuroimmunol. PD SEP PY 2006 VL 178 IS 1-2 BP 149 EP 155 DI 10.1016/j.jneuroim.2006.05.025 PG 7 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 094PI UT WOS:000241251000016 PM 16842863 ER PT J AU Yirmiya, N Rosenberg, C Salomon, S Levi, S Shulman, C Yirmiya, R Ebstein, R AF Yirmiya, N. Rosenberg, C. Salomon, S. Levi, S. Shulman, C. Yirmiya, R. Ebstein, R. TI Association of polymorphism in the IL-1ra gene with autism and pervasive developmental disorders SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Meeting Abstract CT 8th International Conference of Neuroimmunology CY OCT 15-19, 2006 CL Nagoya, JAPAN C1 Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. S Herzog Mem Hosp, Res Dept, Jerusalem, Israel. Hebrew Univ Jerusalem, Dept Child Psychiat, Jerusalem, Israel. Hebrew Univ Jerusalem, Sch Social Work, Jerusalem, Israel. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD SEP PY 2006 VL 178 SU 1 BP 180 EP 180 PG 1 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 099YG UT WOS:000241633101145 ER PT J AU Wiggs, L Stores, G AF Wiggs, L. Stores, G. TI A randomised controlled trial of behavioural intervention for sleeplessness in children with autism spectrum disorders SO JOURNAL OF SLEEP RESEARCH LA English DT Meeting Abstract CT 18th Congress of the European-Sleep-Research-Society CY SEP 12-16, 2006 CL Innsbruck, AUSTRIA SP European Sleep Res Soc C1 Oxford Brookes Univ, Dept Psychol, Oxford OX3 0BP, England. Univ Oxford, Dept Psychiat, Oxford, England. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0962-1105 J9 J SLEEP RES JI J. Sleep Res. PD SEP PY 2006 VL 15 SU 1 BP 83 EP 83 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 076NW UT WOS:000239966000205 ER PT J AU Limoges, RG Bolduc, C Mottron, L AF Limoges, R. Godbout Bolduc, C. Mottron, L. TI Sleep organization correlates with attention and memory in adults with high functioning autism SO JOURNAL OF SLEEP RESEARCH LA English DT Meeting Abstract CT 18th Congress of the European-Sleep-Research-Society CY SEP 12-16, 2006 CL Innsbruck, AUSTRIA SP European Sleep Res Soc C1 Univ Montreal, Neurodev Disorders Program, Montreal, PQ H3C 3J7, Canada. Univ Montreal, Ctr Rech Fernand Seguin, Montreal, PQ H3C 3J7, Canada. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0962-1105 J9 J SLEEP RES JI J. Sleep Res. PD SEP PY 2006 VL 15 SU 1 BP 163 EP 163 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 076NW UT WOS:000239966000443 ER PT J AU Leveille, C Bolduc, C Limoges, E Braun, CJ Mottron, L Godbout, R AF Leveille, C. Bolduc, C. Limoges, E. Braun, C. J. Mottron, L. Godbout, R. TI Wake and REM sleep EEG coherence in adults with high functioning autism SO JOURNAL OF SLEEP RESEARCH LA English DT Meeting Abstract CT 18th Congress of the European-Sleep-Research-Society CY SEP 12-16, 2006 CL Innsbruck, AUSTRIA SP European Sleep Res Soc C1 Univ Montreal, Hop Riviere Prairies, Dept Psychiat, Sleep Lab & Clin,Neurodev Disorders Program, Montreal, PQ, Canada. Hop Riviere Prairies, Ctr Rech Fernand Seguin, Montreal, PQ, Canada. Univ Montreal, Hop Riviere Prairies, Sleep Lab & Clin, Dept Psychol,Neurodev Disorders Program, Montreal, PQ H3C 3J7, Canada. Univ Quebec, Hop Riviere Prairies, Dept Psychol, Sleep Lab & Clin,Neurodev Orders Program, Montreal, PQ H3C 3P8, Canada. Hop Riviere Prairies, Ctr Rech Fernand Seguin, Montreal, PQ, Canada. Univ Quebec, Dept Psychol, Montreal, PQ H3C 3P8, Canada. NR 0 TC 0 Z9 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0962-1105 J9 J SLEEP RES JI J. Sleep Res. PD SEP PY 2006 VL 15 SU 1 BP 164 EP 164 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 076NW UT WOS:000239966000445 ER PT J AU Risi, S Lord, C Gotham, K Corsello, C Chrysler, C Szatmari, P Cook, EH Leventhal, BL Pickles, A AF Risi, Susan Lord, Catherine Gotham, Katherine Corsello, Christina Chrysler, Christina Szatmari, Peter Cook, Edwin H., Jr. Leventhal, Bennett L. Pickles, Andrew TI Combining information from multiple sources in the diagnosis of autism spectrum disorders SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism diagnosis; Autism diagnostic Interview-Revised; Autism Diagnostic Observation Schedule ID PERVASIVE DEVELOPMENTAL DISORDERS; SOCIAL-BEHAVIOR; TWINS AB Background: Standard case criteria are proposed for combined use of the Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule to diagnose autism and to define the broader category of autism spectrum disorders. Method: Single and combined Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule algorithms were compared to best estimate diagnoses in four samples: U.S. (n = 960) and Canadian (n = 232) participants 3 years and older, U.S. participants younger than 36 months (n = 270), and U.S. participants older than 36 months with profound mental retardation (n = 67). Results: Sensitivities and specificities of 80% and higher were obtained when strict criteria for an autism diagnosis using both instruments were applied in the U.S. samples, and 75% or greater in the Canadian sample. Single-instrument criteria resulted in significant loss of specificity. Specificity was poor in the sample with profound mental retardation. Lower sensitivity and specificity were also obtained when proposed criteria for broader spectrum disorders were applied. Conclusions: The Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule make independent, additive contributions to the judgment of clinicians that result in a more consistent and rigorous application of diagnostic criteria. C1 Univ Michigan, Autism & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. McMaster Univ, Offord Ctr Child Studies, Hamilton, ON L8S 4L8, Canada. Univ Illinois, Dept Psychiat, Chicago, IL 60680 USA. Univ Manchester, Manchester M13 9PL, Lancs, England. RP Risi, S (reprint author), UMACC, 1111 E Catherine, Ann Arbor, MI 48109 USA. EM srisi@umich.edu RI Pickles, Andrew/A-9625-2011 OI Pickles, Andrew/0000-0003-1283-0346 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 Constantino JN, 2003, J AM ACAD CHILD PSY, V42, P458, DOI 10.1097/01.CHI.0000046811.95464.21 Dunn G., 2000, STAT PSYCHIAT Elliot C., 1990, DIFFERENTIAL ABILITI Fombonne E, 2005, J CLIN PSYCHIAT, V66, P3 Palferman S, 2001, AM J HUM GENET, V69, P570 Kraemer H. 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Am. Acad. Child Adolesc. Psychiatr. PD SEP PY 2006 VL 45 IS 9 BP 1094 EP 1103 DI 10.1097/01.chi.0000227880.42780.0e PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 078NO UT WOS:000240110700009 PM 16926617 ER PT J AU Vorstman, JAS Morcus, MEJ Duijff, SN Klaassen, PWJ Heineman-de Boer, JA Beemer, FA Swaab, H Kahn, RS van Engeland, H AF Vorstman, Jacob A. S. Morcus, Monique E. J. Duijff, Sasja N. Klaassen, Petra W. J. Heineman-de Boer, Josien A. Beemer, Frits A. Swaab, Hanna Kahn, Rene S. van Engeland, Herman TI The 22q11.2 deletion in children: High rate of autistic disorders and early onset of psychotic symptoms SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE 22q11 deletion syndrome; velocardiofacial syndrome; autism; psychosis; behavioral phenotype ID CARDIO-FACIAL SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHIATRIC-DISORDERS; CHROMOSOME 22Q11; VELOCARDIOFACIAL-SYNDROME; DIAGNOSTIC INTERVIEW; SPECTRUM DISORDERS; CLINICAL-FEATURES; SCHIZOPHRENIA; CHILDHOOD AB Objective: To examine psychopathology and influence of intelligence level on psychiatric symptoms in children with the 22q11.2 deletion syndrome (22q11DS). Method: Sixty patients, ages 9 through 18 years, were evaluated. Assessments followed standard protocols, including structured and semistructured interviews of parents, videotaped psychiatric interview, and intelligence assessment of the child. Intelligence level, psychiatric symptoms, and classification provided the main outcome. Results: High rates of autism spectrum disorders (30 of 60, 50.0%) and psychotic symptoms (16 of 60, 26.7%) were found in this sample. In 7 of 60 (11.7%), the psychotic symptoms interfered with behavior and caused considerable distress. In these cases, the diagnosis of a psychotic disorder was applied. The average age of the children with psychotic symptoms at time of assessment was 14.2 years. Although it is likely that the high rate of psychopathology in this sample is to some extent associated with the lower level of cognitive function, a major effect of the degree of cognitive impairment on psychiatric morbidity was not found. Conclusion: Autism spectrum disorders and subthreshold autistic symptomatology are common in children with 22q11DS. Furthermore, a high rate of psychosis and psychotic symptoms is found in this childhood sample, suggesting an early onset of psychosis in 22q11DS patients. Autistic and psychotic disorders should be considered to be main elements of the behavioral phenotype of 22q11DS children. C1 Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, NL-3508 TA Utrecht, Netherlands. Univ Utrecht, Med Ctr, Dept Pediat Psychol, NL-3508 TA Utrecht, Netherlands. Univ Utrecht, Med Ctr, Dept Med Genet, NL-3508 TA Utrecht, Netherlands. Univ Utrecht, Med Ctr, Dept Psychiat, NL-3508 TA Utrecht, Netherlands. Rudolf Magnus Inst Neurosci, NL-3508 TA Utrecht, Netherlands. RP Vorstman, JAS (reprint author), Childrens Hosp Philadelphia, Abramson Res Ctr, Div Human Genet & Mol Biol, Room 1002,3615 Civ Ctr Blvd, Philadelphia, PA 19104 USA. 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PD SEP PY 2006 VL 45 IS 9 BP 1104 EP 1113 DI 10.1097/01.chi.0000228131.56956.cl PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 078NO UT WOS:000240110700010 PM 16926618 ER PT J AU Scahill, L McDougle, CJ Williams, SK Dimitropoulos, A Aman, MG McCracken, JT Tierney, E Arnold, LE Cronin, P Grados, M Ghuman, J Koenig, K Lam, KSL McGough, J Posey, DJ Ritz, L Swiezy, NB Vitiello, B AF Scahill, Lawrence McDougle, Christopher J. Williams, Susan K. Dimitropoulos, Anastasia Aman, Michael G. McCracken, James T. Tierney, Elaine Arnold, L. Eugene Cronin, Pegeen Grados, Marco Ghuman, Jaswinder Koenig, Kathleen Lam, Kristen S. L. McGough, James Posey, David J. Ritz, Louise Swiezy, Naomi B. Vitiello, Benedetto TI Children's Yale-Brown Obsessive Compulsive Scale modified for pervasive developmental disorders SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; pervasive developmental disorders; repetitive behavior; clinical measures ID ABERRANT BEHAVIOR CHECKLIST; PEDIATRIC PSYCHOPHARMACOLOGY; REPETITIVE BEHAVIORS; AUTISM NETWORK; RESEARCH UNITS; RISPERIDONE; RELIABILITY AB Objective: To examine the psychometric properties of the Children's Yale-Brown Obsessive Compulsive Scales (CYBOCS) modified for pervasive developmental disorders (PDDs). Method: Raters from five Research Units on Pediatric Psychopharmacology (RUPP) Autism Network were trained to reliability. The modified scale (CYBOCS-PDD), which contains only the five Compulsion severity items (range 0-20), was administered to 172 medication-free children (mean 8.2 +/- 2.6 years) with PDD (autistic disorder, n = 152; Asperger's disorder, n = 6; PDD not otherwise specified, n = 14) participating in RUPP clinical trials. Reliability was assessed by intraclass correlation coefficient (ICC)and internal consistency by Cronbach's alpha coefficient. Correlations with ratings of repetitive behavior and disruptive behavior were examined for validity. Results: Eleven raters showed excellent reliability (ICC = 0.97). The mean CYBOCS score was 14.4 +/- 3.86) with excellent internal consistency (alpha = .85). Correlations with other measures of repetitive behavior ranged from r = 0.11 to r = 0.28 and were similar to correlations with measures of irritability (r = 0.24) and hyperactivity (r = 0.25). Children with higher scores on the CYBOCS-PDD had higher levels of maladaptive behaviors and lower adaptive functioning. Conclusions: The five-item CYBOCS-PDD is reliable, distinct from other measures of repetitive behavior, and sensitive to change. C1 Yale Univ, Yale Child Study Ctr, New Haven, CT 06520 USA. RP Scahill, L (reprint author), Yale Univ, Yale Child Study Ctr, POB 207900, New Haven, CT 06520 USA. EM lawrence.scahill@yale.edu CR AMAN MG, 1985, AM J MENT DEF, V89, P492 American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bodfish J.W., 1999, REPETITIVE BEHAV SCA Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 Brown EC, 2002, RES DEV DISABIL, V23, P45, DOI 10.1016/S0891-4222(01)00091-9 CRONBACH LJ, 1951, PSYCHOMETRIKA, V16, P297 Gadow K, 1994, CHILD SYMPTOM INVENT GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1006 Hollander E, 2003, NEUROPSYCHOPHARMACOL, V28, P193, DOI 10.1038/sj.npp.1300021 Jensen JA, 1985, SLOSSON INTELLIGENCE Lam K. S. 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Am. Acad. Child Adolesc. Psychiatr. PD SEP PY 2006 VL 45 IS 9 BP 1114 EP 1123 DI 10.1097/01.chi.0000220854.79144.e7 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 078NO UT WOS:000240110700011 PM 16926619 ER PT J AU Mahone, EM Powell, SK Loftis, CW Goldberg, MC Denckla, MB Mostofsky, SH AF Mahone, E. Mark Powell, Stephanie K. Loftis, Christopher W. Goldberg, Melissa C. Denckla, Martha B. Mostofsky, Stewart H. TI Motor persistence and inhibition in autism and ADHD SO JOURNAL OF THE INTERNATIONAL NEUROPSYCHOLOGICAL SOCIETY LA English DT Article; Proceedings Paper CT 33rd Annual Meeting of the International-Neuropsychological-Society CY FEB 03, 2005 CL St Louis, MO SP Int Neuropsychol Soc DE neuropsychological tests; motor skill; executive function; developmental disorders; child; development ID DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DIAGNOSTIC OBSERVATION SCHEDULE; EXECUTIVE FUNCTIONS; OCULOMOTOR ABNORMALITIES; FRONTAL-LOBE; LEARNING-DISABILITY; RESPONSE-INHIBITION; TOURETTE-SYNDROME; CHILDREN AB The present study compared performance of children with Attention-Deficit/Hyperactivity Disorder (ADHD) and high functioning autism (HFA) with that of controls on 4 tasks assessing 2 components of motor control: motor response inhibition and motor persistence. A total of 136 children (52 ADHD, 24 HFA, 60 controls) ages 7 to 13 years completed 2 measures of motor inhibition (Conflicting Motor Response and Contralateral Motor Response Tasks) and 2 measures of motor persistence (Lateral Gaze Fixation and NEPSY Statue). After controlling for age, IQ, gender, and basic motor speed, children with ADHD performed significantly more poorly than controls on the Conflicting Motor Response and Contralateral Motor Response Tasks, as well as on Statue. In contrast, children with HFA achieved lower scores than controls only on measures of motor persistence, with no concomitant impairment on either motor inhibition task. These results are consistent with prior research that has demonstrated relatively spared motor inhibition in autism. The findings highlight the utility of brief assessments of motor control in delineating the unique neurobehavioral phenotypes of ADHD and HFA. C1 Kennedy Krieger Inst, Dept Neuropsychol, Baltimore, MD 21231 USA. 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Int. Neuropsychol. Soc. PD SEP PY 2006 VL 12 IS 5 BP 622 EP 631 DI 10.1017/S1355617706060814 PG 10 WC Clinical Neurology; Neurosciences; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA 081ZE UT WOS:000240355300004 PM 16961943 ER PT J AU Johnson, SA Yechiam, E Murphy, RR Queller, S Stout, JC AF Johnson, Shannon A. Yechiam, Eldad Murphy, Robin R. Queller, Sarah Stout, Julie C. TI Motivational processes and autonomic responsivity in Asperger's disorder: Evidence from the Iowa Gambling Task SO JOURNAL OF THE INTERNATIONAL NEUROPSYCHOLOGICAL SOCIETY LA English DT Article; Proceedings Paper CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc DE autism; decision-making; choice behavior; galvanic skin response; learning; mathematical model ID HIGH-FUNCTIONING AUTISM; HUMAN DECISION-MAKING; PREFRONTAL CORTEX; DIAGNOSTIC INTERVIEW; CHILDREN; PERFORMANCE; AMYGDALA; EMOTION; DAMAGE; ATTENTION AB Asperger's disorder (ASP), like other autism spectrum disorders, is associated with altered responsiveness to social stimuli. This study investigated learning and responsiveness to nonsocial, but motivational, stimuli in ASP. We examined choice behavior and galvanic skin conductance responses (SCRs) during the Iowa Gambling Task (IGT; Bechara et al., 1994) in 15 adolescents and young adults with ASP and 14 comparison subjects. We examined aspects of learning, attention to wins and losses, and response style with a formal cognitive model, the Expectancy-Valence Learning model (Busemeyer & Stout, 2002). The ASP group did not differ from the comparison group in proportions of selections from advantageous decks. However, ASP participants showed a distinct pattern of selection characterized by frequent shifts between the four IGT decks, whereas comparison participants developed clear deck preferences. SCR results showed some evidence of reduced responsiveness in the ASP group during the IGT. Results from the cognitive model indicated that, in contrast to the comparison group, the ASP group's selections were less consistent with the motivational significance they assigned to decks. Findings are discussed in the context of the neurobiological substrates associated with IGT performance. C1 Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN 47405 USA. RP Stout, JC (reprint author), Indiana Univ, Dept Psychol & Brain Sci, 1101 E 10th St, Bloomington, IN 47405 USA. 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PD SEP PY 2006 VL 12 IS 5 BP 668 EP 676 DI 10.1017/S1355617706060802 PG 9 WC Clinical Neurology; Neurosciences; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA 081ZE UT WOS:000240355300009 PM 16961948 ER PT J AU Spiegel, EK Colman, RF Patterson, D AF Spiegel, Erin K. Colman, Roberta F. Patterson, David TI Adenylosuccinate lyase deficiency SO MOLECULAR GENETICS AND METABOLISM LA English DT Review DE autism; psychomotor retardation; purine biosynthesis; enzyme; succinylpurines ID 3-CARBOXY-CIS,CIS-MUCONATE LACTONIZING ENZYME; PURINE NUCLEOTIDE CYCLE; BACILLUS-SUBTILIS; CRYSTAL-STRUCTURE; INBORN ERROR; ACTIVE-SITE; ADSL GENE; MUTATION; IDENTIFICATION; EXPRESSION AB Adenylosuccinate lyase deficiency is a disease of purine metabolism which affects patients both biochemically and behaviorally. The symptoms are variable and include psychomotor retardation, autistic features, hypotonia, and seizures. Patients also accumulate the substrates of ADSL in body fluids. Both the presence of normal levels of ADSL enzyme activities in some patient tissues and the absence of a clear correlation between mutations, biochemistry, and behavior show that the system has unexplored biochemical and/or genetic complexity. It is unclear whether the pathological mechanisms of this disease result from a deficiency of purines, a toxicity of intermediates, or perturbation of another pathway or system. A patient with autistic features and mild psychomotor delay carries two novel mutations in this gene, E80D and D87E. The creation of a mouse model of this disease will be an important step in elucidating the if? vivo mechanisms of the disease. Mice carrying mutations that cause ADSL deficiency in humans will be informative as to the effects of these mutations both during embryogenesis and on the brain, possibly leading to therapies for this disease in the future. (c) 2006 Elsevier Inc. All rights reserved. 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TI Autism and environmental genomics SO NEUROTOXICOLOGY LA English DT Article; Proceedings Paper CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res DE autism; genetics; environmental genomics; toxicogenomics; systems biology; bioinformatics; genomics; immune ID TOXICOGENOMICS DATABASE CTD; SPECTRUM DISORDERS; GENE-EXPRESSION; EPIGENETIC REGULATION; SOCIAL COMMUNICATION; CHANGING PREVALENCE; CONGENITAL-RUBELLA; LIPID-PEROXIDATION; OXIDATIVE STRESS; CANDIDATE GENES AB Autism spectrum disorders (ASD) are defined by behavior and diagnosed by clinical history and observation but have no biomarkers and are presumably, etiologically and biologically heterogeneous. Given brain abnormalities and high monozygotic concordance, ASDs have been framed as neurobiologically based and highly genetic, which has shaped the research agenda and in particular criteria for choosing candidate ASD genes. Genetic studies to date have not uncovered genes of strong effect, but a move toward "genetic complexity" at the neurobiological level may not suffice, as evidence of systemic abnormalities (e.g. gastrointestinal and immune), increasing rates and less than 100% monozygotic concordance support a more inclusive refraining of autism as a multisystern disorder with genetic influence and environmental contributors. We review this evidence and also use a bioinformatic approach to explore the possibility that "environmentally responsive genes" not specifically associated with the nervous system, but potentially associated with systemic changes in autism, have not hitherto received sufficient attention in autism genetics investigations. We overlapped genes from NIEHS Environmental Genome Project, the Comparative Toxicogenomics Database, and the SeattleSNPs database of genes relevant to the human immune and inflammatory response with linkage regions identified in published autism genome scans. We identified 135 genes in overlap regions, of which 56 had never previously been studied in relation to autism and 47 had functional SNPs (in coding regions). Both our review and the bioinformatics exercise support the expansion of criteria for evaluating the relevance of genes to autism risk to include genes related to systemic impact and environmental responsiveness. This review also suggests the utility of environmental genomic resources in highlighting the potential relevance of particular genes within linkage regions. Environmental responsiveness and systems impacts consistent with system-wide findings in autism are thus supported as important considerations in identifying the numerous and complex modes of gene-environment interaction in autism. (C) 2006 Elsevier Inc. All rights reserved. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Morphometr Anal, Charlestown, MA 02129 USA. Boston Univ, Boston, MA 02215 USA. Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. Univ Arkansas Med Sci, Dept Pediat, Little Rock, AR 72205 USA. RP Herbert, MR (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Morphometr Anal, 149 13th St,Room 6012, Charlestown, MA 02129 USA. 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Segal, Jeffrey Aschner, Michael TI Cultured lymphocytes from autistic children and non-autistic siblings up-regulate heat shock protein RNA in response to thimerosal challenge SO NEUROTOXICOLOGY LA English DT Article; Proceedings Paper CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res DE autism; ethyl mercury; metallothionein; micorarrays ID PERIPHERAL-BLOOD LYMPHOCYTES; METALLOTHIONEIN INDUCTION; ASTROCYTE CULTURES; INDUCED APOPTOSIS; GENE-EXPRESSION; NULL MICE; METHYLMERCURY; MERCURY; CELLS; ZINC AB There are reports suggesting that some autistic children are unable to mount an adequate response following exposure to environmental toxins. This potential deficit, coupled with the similarity in clinical presentations of autism and some heavy metal toxicities, has led to the suggestion that heavy metal poisoning might play a role in the etiology of autism in uniquely susceptible individuals. Thimerosal, an anti-microbial preservative previously added routinely to childhood multi-dose vaccines, is composed of 49.6% ethyl mercury. Based on the levels of this toxin that children receive through routine immunization schedules in the first years of life, it has been postulated that thimerosal may be a potential triggering mechanism contributing to autism in susceptible individuals. One potential risk factor in these individuals may be an inability to adequately upregulate metallothionein (MT) biosynthesis in response to presentation of a heavy metal challenge. To investigate this hypothesis, cultured lymphocytes (obtained from the Autism Genetic Resource Exchange, AGRE) from autistic children and non-autistic siblings were challenged with either 10 mu M ethyl mercury, 150 mu M zinc, or fresh media (control). Following the challenge, total RNA was extracted and used to query "whole genome" DNA microarrays. Cultured lymphocytes challenged with zinc responded with an impressive up-regulation of MT transcripts (at least nine different MTs were over-expressed) while cells challenged with thimerosal responded by up-regulating numerous heat shock protein transcripts, but not MTs. Although there were no apparent differences between autistic and non-autistic sibling responses in this very small sampling group, the differences in expression profiles between those cells treated with zinc versus thimerosal were dramatic. Determining cellular response, at the level of gene expression, has important implications for the understanding and treatment of conditions that result from exposure to neurotoxic compounds. (C) 2006 Elsevier Inc. All rights reserved. C1 Wake Forest Univ, Sch Med, Dept Physiol & Pharmacol, Winston Salem, NC 27156 USA. Vanderbilt Univ, Med Ctr, Dept Pediat, Nashville, TN 37232 USA. Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA. Vanderbilt Univ, Med Ctr, Kennedy Ctr, Nashville, TN 37232 USA. RP Walker, SJ (reprint author), Dept Physiol & Pharmacol, 115 S Chestnut St,PTCRC Bldg, Winston Salem, NC 27101 USA. 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SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Autism Soc Amer, Bethesda, MD USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 877 EP 878 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800031 ER PT J AU Herbert, MR Russo, J Yang, S Roohi, J Blaxill, M Kahler, S Mccoy, L Ziegler, DA Hatchwell, E AF Herbert, Martha R. Russo, J. P. Yang, S. Roohi, J. Blaxill, M. Kahler, S. G. McCoy, L. Ziegler, D. A. Hatchwell, E. TI Autism, genes and the environment. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, CMA & Pediat Neurol, Charlestown, MA 02129 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 877 EP 877 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800029 ER PT J AU Harry, GJ Carson, M AF Harry, G. Jean Carson, Monica TI Session III-B: Developmental effects on the immune system: Implications for autism and neurodevelopmental disorders SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 880 EP 880 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800038 ER PT J AU McMahon, W AF McMahon, William TI A case-control study of antibodies to central nervous system proteins and measles virus in children with autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Univ Utah, Dept Neurol, Salt Lake City, UT 84112 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 881 EP 881 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800043 ER PT J AU Pardo-Villamizar, C AF Pardo-Villamizar, Carlos TI Neuroinflammatory and neuroglial CNS responses in autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 881 EP 881 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800042 ER PT J AU Stigler, KA AF Stigler, Kimberly A. TI Autism and the immune system: An overview. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Indiana Sch Med, Indianapolis, IN USA. NR 0 TC 1 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 881 EP 881 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800041 ER PT J AU Van de Water, J AF Van de Water, Judy TI Suboptimal IGG response to bacterial vaccine antigens in patients with autism spectrum disorder (ASD). SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 881 EP 882 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800044 ER PT J AU Croen, L AF Croen, Lisa TI Maternal immune status during pregnancy and childhood autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Kaiser Permanente Div Res, Oakland, CA USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 882 EP 882 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800045 ER PT J AU Kane, PC Braccia, D Cartaxo, A Kane, E AF Kane, P. C. Braccia, D. Cartaxo, A. Kane, E. TI Clearance of neurotoxins by phospholipid emulsion in autism and PDD. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Haverford Wellness Ctr, Havertown, PA 19083 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 883 EP 883 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800047 ER PT J AU Crawley, JN AF Crawley, Jacqueline N. TI Defining mouse behaviors related autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 NIMH, Bethesda, MD 20892 USA. Univ N Carolina, Sch Med, Neurodev Disorders Res Ctr, Chapel Hill, NC USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 892 EP 892 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800070 ER PT J AU James, SJ Melnyk, S Jernigan, S AF James, S. J. Melnyk, S. Jernigan, S. TI Oxidative stress in children with autism: Metabolic biomarkers and genetic polymorphisms. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Univ Arkansas Med Sci, Dept Pediat, Sch Med, Little Rock, AR 72205 USA. Arkansas Childrens Hosp, Res Inst, Little Rock, AR 72202 USA. NR 0 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 893 EP 894 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800074 ER PT J AU Piven, J AF Piven, Joe TI Defining the autism and broad autism phenotypes. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 894 EP 894 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800075 ER PT J AU Herbert, MR Russo, JP Yang, S Roohi, J Blaxill, M Kahler, SG McCoy, L Ziegler, DA Hatchwell, E AF Herbert, M. R. Russo, J. P. Yang, S. Roohi, J. Blaxill, M. Kahler, S. G. McCoy, L. Ziegler, D. A. Hatchwell, E. TI Autism and environmental genomics. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, CMA & Pediat Neurol, Charlestown, MA USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 906 EP 907 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800099 ER PT J AU Ogawa, T Kuwagata, M Shioda, S AF Ogawa, T. Kuwagata, M. Shioda, S. TI A new developmental neurotoxicity study focusing on the fetal brain: Evaluation of a rat autism model induced by valproate and thalidomide. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res C1 Showa Univ, Sch Med, Dept Anat, Tokyo 142, Japan. FDSC, Hatano Res Inst, Kanagawa, Japan. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 907 EP 907 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800100 ER PT J AU Walker, SJ AF Walker, S. J. TI Cultured lymphocytes from autistic patients and non-autisitc siblings upregulate heat shock protein RNA in response to thimerosal challenge. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res DE autism; lymphocytes; thimerosal C1 Wake Forest Univ, Dept Physiol & Pharmacol, Winston Salem, NC 27109 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 907 EP 907 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800101 ER PT J AU Ogawa, T Kuwagata, M Shioda, S AF Ogawa, T. Kuwagata, M. Shioda, S. TI A new developmental neurotoxicity study focusing on the fetal brain: Evaluation of a rat autism model induced by valproate and thalidomide. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res DE fetal brain; valproate; developmental neurotoxicity C1 Showa Univ, Sch Med, Dept Anat, Tokyo 142, Japan. FDSC, Hatano Res Inst, Kanagawa, Japan. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 911 EP 911 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800111 ER PT J AU Cheh, MA Millonig, JH Jacobsen, E Ming, X Wagner, GC AF Cheh, M. A. Millonig, J. H. Jacobsen, E. Ming, X. Wagner, G. C. TI Animal model of autism using En2(-l-) mice. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 22nd International Neurotoxicology Conference CY SEP 11-14, 2005 CL Res Triangle Park, NC SP Natl Inst Environm Hlth Sci, USA Med Res & Mat Command, USA Res Inst Environm Med, Ctr Hlth Res, Res Fdn Hlth & Environm Effect, Aurism Soc Amer, CDC/Natl Ctr Environm Hlth & ATSDR, BUG/NIEHS Superfund Basic Res Program, NIH/Natl Inst Neurol Disorder & Stroke, March Dimes Birth Defects Fdn, Manganese Hlth Res Program, Elsevier Sci, Elect Power Res Inst, US Tuna Fdn, Amer Chem Council, Polychlorinated Biphenyls Panel, Ctr Toxicol & Environm Hlth, Charles River DDS, Argus Div, NIH/Natl Inst Child Hlth & Human Dev, Soc Toxicol, Arkansas Childrens Hosp, FDA/Natl Ctr Toxicol Res DE animal model; autism; engrailed-2 C1 Rutgers State Univ, Dept Neurosci, New Brunswick, NJ 08903 USA. Rutgers State Univ, Dept Psychol, New Brunswick, NJ 08903 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurosci, Newark, NJ 07103 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SEP PY 2006 VL 27 IS 5 SI SI BP 928 EP 928 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 082SZ UT WOS:000240408800154 ER PT J AU Stodgell, CJ Ingram, JL O'Bara, M Tisdale, BK Nau, H Rodier, PM AF Stodgell, Christopher J. Ingram, Jennifer L. O'Bara, Melanie Tisdale, Barbara K. Nau, Heinz Rodier, Patricia M. TI Induction of the homeotic gene Hoxa1 through valproic acid's teratogenic mechanism of action SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Article DE development; autism; teratogens; rat; gene expression; 4-vn-VPA; IE-VPA; retinoic acid ID NEURAL-TUBE DEFECTS; PERVASIVE DEVELOPMENTAL DISORDERS; FETAL ANTICONVULSANT SYNDROME; RETINOIC ACID; HISTONE DEACETYLASE; ANTIEPILEPTIC DRUGS; PRESCHOOL-CHILDREN; A218G POLYMORPHISM; ALLELIC VARIANTS; AUTISM AB Background: Valproic acid (VPA) exposure in utero has been associated with an increased risk of both neural tube defects and autism spectrum disorders (ASDs). The terata induced by VPA suggest interference with pattern formation. Retinoic acid produces similar terata and is known to act in part by increasing the expression of Hoxa1. We tested the hypotheses that exposure to VPA would alter the expression of Hoxal in rat embryos during times of normal Hoxal expression (d10.5-13.5) and that exposure at earlier and later stages would induce inappropriate expression. Method: Hoxa1 expression levels were determined by real-time PCR in individual embryos 1 h after exposure on gestational d10, 12, 13, 14, or 15. Additionally, teratogenic (4-yn-VPA) and nonteratogenic analogs of VPA (IE-VPA), retinoic acid (RA), and saline were compared for effects on Hoxal expression on d12. Embryos were allowed to develop for 1, 2, 4, 6, or 24 h, to follow the time course of effects. Results: In utero exposure to VPA on gestational d10 and on d12-14 significantly increased the level of Hoxal expression compared to saline-exposed embryos at developmental ages prior to, during and after the normal expression period for this gene. On gestational d12, exposures to VPA and 4-yn-VPA significantly increased Hoxal expression at all sacrifice times, compared to saline-exposed embryos. RA significantly elevated Hoxal expression at all time points except 24-h post-treatment. The nonteratogenic VPA analog, IE-VPA, did not affect Hoxal expression. Conclusions: VPA and 4-yn-VPA exposures elevated Hoxal mRNA during its normal expression period and induced expression outside of the normal period. This may explain, in part, how VPA disrupts development. Published by Elsevier Inc. C1 Univ Rochester, Sch Med & Dent, Dept Obstet & Gynecol, Rochester, NY 14642 USA. Univ Hannover, Ctr Food Sci, Dept Food Toxicol, D-30167 Hannover, Germany. RP Stodgell, CJ (reprint author), Univ Rochester, Sch Med & Dent, Dept Obstet & Gynecol, Rochester, NY 14642 USA. 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Teratol. PD SEP-OCT PY 2006 VL 28 IS 5 BP 617 EP 624 DI 10.1016/j.ntt.2006.08.004 PG 8 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA 115OG UT WOS:000242743000011 PM 16989981 ER PT J AU Padilla, FV de la Torre, AM AF Padilla, F. Viguria de la Torre, A. Mijan TI Pica: The portrait of a little known clinical entity SO NUTRICION HOSPITALARIA LA English DT Review DE pica, geophagia; mental retardation; eating disorder; review ID MENTALLY-RETARDED ADULTS; IRON-DEFICIENCY ANEMIA; NEUROPHARMACOLOGICAL MECHANISMS; ZINC SUPPLEMENTATION; RAPUNZEL SYNDROME; ANTIEMETIC DRUGS; PREGNANT-WOMEN; ANIMAL-MODEL; GEOPHAGY; RATS AB Pica is a eating disorder, of the eating behavior in childhood. It is defined as the persistent intake of non-nutritional substances for at least one month, in an inappropriate way from an evolutionary perspective, and provided that its practice is not culturally banned. Many animal species, including primates, have this behavior. Documented from antiquity, in most cases it has been considered a symptom of another related disorder rather than as independent condition. Its prevalence is unknown. It is mainly described in mentally disabled people, pregnant women, autism, mentally ill patients, children, and others. The ingestion of earth, ice, starch, ropes, wood, and other products has been observed, although some authors also include the obsessive and reiterative consumption of eatable substances. Geophagia is considered a cultural phenomenon, although sometimes may lead to disease, and an form of paleomedicine or paleonutrition. The etiology of pica is unknown and it has no markers. Sensitive, digestive, nutritional, psychological, and psychiatric factors have been implicated in its origin and maintenance. Although the morbimortality is unknown and difficult to study, we may highlight intoxications, parasitic diseases, and surgical abdomen with serious complications. 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Low maternal plasma serotonin may contribute to abnormal brain development in autism. In this study, plasma serotonin levels in autism mothers and control mothers of typically developing children were compared, and plasma serotonin levels in children with autism (n = 17) and their family members were measured. Plasma serotonin levels in autism mothers were significantly lower than in mothers of normal children (P = 0.002). Plasma serotonin levels correlated between autism mothers and their children, but differed between autistic children and their fathers (P = 0.028) and siblings (P = 0.063). Low maternal plasma serotonin may be a risk factor for autism through effects on fetal brain development. (c) 2006 by Elsevier Inc. All rights reserved. C1 Kennedy Krieger Inst, Dept Neurol & Dev Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Univ Tennessee, Med Ctr, Dev & Genet Ctr, Knoxville, TN 37920 USA. Univ Tennessee, Med Ctr, Dept Anesthesiol, Knoxville, TN 37920 USA. RP Zimmerman, AW (reprint author), Kennedy Krieger Inst, Dept Neurol & Dev Med, 707 N Broadway, Baltimore, MD 21205 USA. 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Unfortunately, children with autism represent an underserved patient population. Parents often make treatment decisions with insufficient information and report problems in establishing and maintaining treatment programs. This practice review asserts that psychologists, including those without professional certification or coursework in ABA, are in a unique position to assist affected children and their families. Psychologists can provide critical information about evidence-based treatment; offer assistance in overcoming barriers to intensive treatment, including personnel selection; and provide ongoing support to family members. Case examples also illustrate how psychologists can help families address specific barriers to intensive treatment. C1 Penn State Univ, Dept Psychol, Berks Coll, University Pk, PA 16802 USA. RP Hillman, J (reprint author), Appl Psychol Program, POB 7009, Reading, PA USA. 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Department of Health and Human Services, 1999, MENT HLTH REP SURG G Volkmar FR, 2004, J CHILD PSYCHOL PSYC, V45, P135, DOI 10.1046/j.0021-9630.2003.00317.x Weisz JR, 2005, AM PSYCHOL, V60, P628, DOI 10.1037/0003-066X.60.6.628 NR 42 TC 6 Z9 6 PU AMER PSYCHOLOGICAL ASSOC, DIV PSYCHOTHERAPY PI CORAL GABLES PA 1390 SOUTH DIXIE HIGHWAY, STE 2222, CORAL GABLES, FL 33146-2946 USA SN 0033-3204 J9 PSYCHOTHERAPY JI Psychotherapy PD FAL PY 2006 VL 43 IS 3 BP 349 EP 358 DI 10.1037/0033-3204.43.3.349 PG 10 WC Psychology, Clinical SC Psychology GA 089AP UT WOS:000240852600013 PM 22122105 ER PT J AU Cassell, JA Leach, M Poltorak, MS Mercer, CH Iversen, A Fairhead, JR AF Cassell, J. A. Leach, M. Poltorak, M. S. Mercer, C. H. Iversen, A. Fairhead, J. R. TI Is the cultural context of MMR rejection a key to an effective public health discourse? SO PUBLIC HEALTH LA English DT Article DE MMR; choice; homeopathy; vitamin K; survey ID RUBELLA VACCINE; IMMUNIZATION; MEASLES; MUMPS; RISK; STATEMENT; AUTISM AB Objectives: (1) To explore the social and cultural influences, and health beliefs associated with low uptake of MMR (meastes, mumps and rubella vaccine). (2) To describe and explore the prevalence of health beliefs associated with noncompliance with MMR, with a view to improving the personal relevance and impact of information for parents, in the context of persisting low uptake following public controversy. Methods: We undertook a survey of mothers' experiences of and attitudes to the MMR, developed through ethnographic study, which was linked to maternal and child information on the Child Health Database in Brighton, England. Results: Mothers interpret MMR risk through concepts of child health embedded in family health history, with a majority both of compliers and non-compliers holding that each child's immune system is unique. Cultural 'risk factors' for non-compliance relate strongly to the use of complementary healthcare, such as homeopathy, with evidence that rejection of vitamin K is associated with MMR non-compliance. Forty per cent, both of compliers and non-compliers, did not consider the possible benefits to other children of MMR. Conclusions: These findings have paradoxical and challenging consequences for the promotion of immunization in the policy context of increasing emphasis on healthy choices. They demonstrate the need for immunization information that acknowledges and addresses lay concepts of immunity. (c) 2006 The Royal Institute of Public Health. Published by Elsevier Ltd. All rights reserved. C1 UCL Royal Free & Univ Coll Med Sch, Dept Primary Care & Populat Sci, London NW2 2PF, England. Univ Sussex, Inst Dev Studies, Brighton, E Sussex, England. Univ Sussex, Dept Anthropol, Brighton, E Sussex, England. RP Cassell, JA (reprint author), UCL Royal Free & Univ Coll Med Sch, Dept Primary Care & Populat Sci, Rowland Hill St, London NW2 2PF, England. 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Levels of disturbance were compared firstly in individuals with and without features of autism as assessed by the DASH-II, and secondly in individuals with varying severities of autism. In both cases levels of ability and overall severity of behaviour disorder were comparable across groups. Individuals with autistic features were found to have significantly higher scores than nonautistic individuals on the DASH-II organic disorder, anxiety, mania, PDD/autism and stereotypies subscales. When participants with autistic features were separated into groups of severe and moderate autism and compared with nonautistic participants, significant effects of group were found for scores on the anxiety, mood, mania, PDD/autism, schizophrenia and stereotypies subscales. Scheffe tests were conducted to further evaluate between-group differences. Item analysis showed seven DASH-II items to have a 30% or more difference between levels of endorsement in autistic and nonautistic individuals, with six further items showing a 20% or greater difference in levels of endorsement. Findings are compared to those from previous research and implications for the conceptualisation of emotional and behavioural disorders in individuals with autism are discussed. (c) 2005 Elsevier Ltd. All rights reserved. C1 Nottinghamshire Healthcare NHS Trust, Community Learning Disabil Team, Worksop S80 2JD, Notts, England. Hesley Grp, Doncaster, England. Univ Leicester, Sch Psychol, Leicester, Leics, England. RP Hill, J (reprint author), Nottinghamshire Healthcare NHS Trust, Community Learning Disabil Team, 53,Cheapside, Worksop S80 2JD, Notts, England. 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TI Diagnosis and treatment of brain creatine deficiency syndromes SO REVISTA DE NEUROLOGIA LA English DT Review DE autism; brain creatine deficiency; creatine; epilepsy; guanidinoacetate; mental retardation ID GUANIDINOACETATE-METHYLTRANSFERASE DEFICIENCY; ARGININE-GLYCINE AMIDINOTRANSFERASE; LINKED MENTAL-RETARDATION; TRANSPORTER GENE SLC6A8; MOUSE-CHROMOSOME 10; GAMT DEFICIENCY; INBORN ERROR; MOLECULAR CHARACTERIZATION; ENZYME ASSAY; METABOLISM AB Aim. To review the clinical, biochemical and genetic aspects of brain creatine deficiency syndromes, as well as the therapeutic options available. Development. Brain creatine deficiency syndrome has recently been described as a series of inborn errors of metabolism that I affect the synthesis and transport of creatine. Three metabolic defects are known: two affect synthesis -guanidinoacetate methyltransferase (GAMT) and arginine:glycine amidinotransferase (AGAT)- and one affects the transport of creatine. Clinically, these patients can display mental retardation, language disorders, epilepsy, autistic behaviour, neurological impairment and movement disorders. After the clinical selection, the different defects can be identified by a biochemical study involving the analysis of metabolites in biological fluids (guanidinoacetate and creatine/creatinine ratio). Before continuing with the molecular studies, it is important to confirm the deficiency of brain creatine by means of magnetic resonance imaging with spectroscopy. Diagnostic confirmation of AGAT and GAMT deficits is carried out by determining the enzymatic activity in fibroblasts or lymphoblasts, or the incorporation of creatine in the case of studies of transport defects. The study of mutations in AGAT, GAMT (autosomal recessive inheritance) and SLC6A8.(X-linked) genes completes the diagnosis. Conclusions. Brain creatine deficiency syndromes are mainly associated to mental retardation and autism. GAMT and AGAT deficiencies respond to treatment with creatine, whereas patients with transport defects do not respond to this therapy; new therapeutic approaches are therefore being evaluated for this disease. C1 Hosp Sant Joan Deu, Serv Bioquim, E-08950 Barcelona, Spain. Hosp Sant Joan Deu, Serv Neuropediat, E-08950 Barcelona, Spain. Corp Sanitaria Clin, Inst Bioquim Clin, Barcelona, Spain. RP Artuch, R (reprint author), Hosp Sant Joan Deu, Serv Bioquim, Passeig Sant Joan Deu 2, E-08950 Barcelona, Spain. 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Csibra, Gergely TI The development and neural basis of referential gaze perception SO SOCIAL NEUROSCIENCE LA English DT Article ID EVENT-RELATED POTENTIALS; SUPERIOR TEMPORAL SULCUS; BIOLOGICAL MOTION PERCEPTION; EYE-GAZE; SOCIAL-PERCEPTION; UNIQUE MORPHOLOGY; HUMAN INFANTS; AUTISM; CHILDREN; BRAIN AB Infants are sensitive to the referential information conveyed by others' eye gaze, which could be one of the developmental foundations of theory of mind. To investigate the neural correlates of gaze-object relations, we recorded ERPs from adults and 9-month-old infants while they watched scenes containing gaze shifts either towards or away from the location of a preceding object. In adults, object-incongruent gaze shifts elicited enhanced ERP amplitudes over the occipito-temporal area (N330). 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Neurosci. PD SEP-DEC PY 2006 VL 1 IS 3-4 BP 220 EP 234 DI 10.1080/17470910600989797 PG 15 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QX UT WOS:000252245100007 PM 18633789 ER PT J AU Perner, J Aichhorn, M Kronbichler, M Staffen, W Ladurner, G AF Perner, Josef Aichhorn, Markus Kronbichler, Martin Staffen, Wolfgang Ladurner, Gunther TI Thinking of mental and other representations: The roles of left and right temporo-parietal junction SO SOCIAL NEUROSCIENCE LA English DT Article ID FALSE BELIEFS; NEUROPSYCHOLOGICAL EVIDENCE; MIND IMPAIRMENTS; WORKING-MEMORY; FMRI; LOBE; PRESCHOOLERS; AUTISM; PHOTOGRAPHS; PERSPECTIVE AB Adopting new versions of the false belief and "false" photo vignettes used by Saxe & Kanwisher (2003) we were able to show activation in all five areas previously reported. Activations by added false sign and temporal change control vignettes in these areas showed that the right temporo-parietal junction (TPJR) is specifically associated with processing mental states like belief. In contrast, TPJ-L was also activated by false signs suggesting an association with processing perspective differences for mental and non-mental objects in line with work on visual perspective tasks. A similar, but less clearly interpretable pattern of activations was also found in the middle temporal gyrus, precuneus and in the MPFC. These results are discussed in relation to findings in normal development where false belief and false sign tasks associate more strongly with each other than does each of them with the "false" photo task. C1 [Perner, Josef] Salzburg Univ, Dept Psychol, A-5020 Salzburg, Austria. [Kronbichler, Martin; Staffen, Wolfgang; Ladurner, Gunther] Paracelsus Privat Med Univ, Salzburg, Austria. 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Neurosci. PD SEP-DEC PY 2006 VL 1 IS 3-4 BP 245 EP 258 DI 10.1080/17470910600989896 PG 14 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QX UT WOS:000252245100009 PM 18633791 ER PT J AU Mazzola, F Seigal, A MacAskill, A Corden, B Lawrence, K Skuse, DH AF Mazzola, Francesca Seigal, Anna MacAskill, Andrew Corden, Ben Lawrence, Kate Skuse, David H. TI Eye tracking and fear recognition deficits in Turner syndrome SO SOCIAL NEUROSCIENCE LA English DT Article ID X-LINKED GENES; FACIAL EXPRESSIONS; AMYGDALA RESPONSES; BEHAVIOR PROBLEMS; AUTISM; FACE; FIXATION; GIRLS; PATTERNS; CHILDREN AB Turner syndrome (TS) is a chromosomal disorder of X-monosomy in females. A minority have impaired social responsiveness, poor discrimination of facial emotions (especially fear), and abnormal amygdalacortical connectivity. We tested the hypothesis that abnormal gaze fixation, especially with the eye region of faces, would be associated with these features, in a similar pattern to that seen in subjects with autism. Furthermore, since these features tend to be more striking in TS women whose X chromosome is maternal in origin, we also predicted that there may be a difference within the Turner's group according to parental origin of the single X. Adults with 45,X karyotype and age and IQ matched 46,XX women were recruited and tested. Facial fear recognition was significantly worse in 45,X females than controls, but there were no group differences according to parental origin of their single X chromosome. Subsequently, we tested 45,X and 46,XX women using a remote eye-tracking device, as they viewed photographs of emotional human faces. Striking differences in scanpaths were found between the TS and controls, and within the TS group, but not according to parental origin of the X chromosome. 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Neurosci. PD SEP-DEC PY 2006 VL 1 IS 3-4 BP 259 EP 269 DI 10.1080/17470910600989912 PG 11 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QX UT WOS:000252245100010 PM 18633792 ER PT J AU Leslie, AM Mallon, R DiCorcia, JA AF Leslie, Alan M. Mallon, Ron DiCorcia, Jennifer A. TI Transgressors, victims, and cry babies: Is basic moral judgment spared in autism? SO SOCIAL NEUROSCIENCE LA English DT Article ID TEMPORO-PARIETAL JUNCTION; NORMAL-CHILDREN; FALSE BELIEF; MIND; COMMUNICATION; PERFORMANCE; PRESCHOOL; DEFICITS AB Human social intelligence comprises a wide range of complex cognitive and affective processes that appear to be selectively impaired in autistic spectrum disorders. The study of these neuro-developmental disorders and the study of canonical social intelligence have advanced rapidly over the last twenty years by investigating the two together. Specifically, studies of autism have provided important insights into the nature of "theory of mind" abilities, their normal development and underlying neural systems. At the same time, the idea of impaired development of the neurocognitive mechanisms underlying "theory of mind" has shed new light on the nature of autistic disorders. This general approach is not restricted to the study of impairments but extends to mapping areas of social intelligence that are spared in autism. Here we investigate basic moral judgment and find that it appears to be substantially intact in children with autism who are severely impaired in "theory of mind". At the same time, we extend studies of moral reasoning in normal development by way of a new control task, the "cry baby" task. Cry baby scenarios, in which the distress of the victim is "unreasonable" or "unjustified," do not elicit moral condemnation from normally developing preschoolers or from children with autism. 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PD SEP-DEC PY 2006 VL 1 IS 3-4 BP 270 EP 283 DI 10.1080/17470910600992197 PG 14 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QX UT WOS:000252245100011 PM 18633793 ER PT J AU Sabbagh, MA Flynn, J AF Sabbagh, Mark A. Flynn, Jessica TI Mid-frontal EEG alpha asymmetries predict individual differences in one aspect of theory of mind: Mental state decoding SO SOCIAL NEUROSCIENCE LA English DT Article ID LANGUAGE COMPREHENSION; ASPERGER-SYNDROME; AFFECTIVE STYLE; NEURAL SYSTEMS; AUTISM; BRAIN; DEPRESSION; PHENOTYPE; RECOGNITION; ACTIVATION AB Mental state decoding is the aspect of theory-of-mind (TOM) reasoning that requires individuals to make judgments about others' mental states based solely on immediately available information. We investigated whether individual differences in resting, task-independent frontal EEG alpha asymmetries predicted performance on the "Mind in the Eyes" (MIE) task, which is an established measure of mental state decoding skills. 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SO SOCIAL NEUROSCIENCE LA English DT Article ID HIGH-FUNCTIONING AUTISM; FRONTAL-LOBE DAMAGE; FALSE-BELIEF; NEUROPSYCHOLOGICAL EVIDENCE; ASPERGER-SYNDROME; EYE GAZE; FRONTOTEMPORAL DEMENTIA; SOCIAL COGNITION; JOINT ATTENTION; YOUNG-CHILDREN AB Twenty years ago, Baron-Cohen and colleagues argued that autistic performance on false belief tests was explained by a deficit in metarepresentation. Subsequent research moved from the view that the mind has a domain-general capacity for metarepresentation to the view that the mind has a domain-specific mechanism for metarepresentation of mental states per se, i.e., the theory of mind mechanism (ToMM). We argue that 20 years of data collection in lesion patients and children with autism supports a more parsimonious view closer to that of the 1985 paper. Lower-level domain-specific mechanisms -e.g., tracking gaze, joint attention -interacting with higher-level domain-general mechanisms for metarepresentation, recursion, and executive function can account for observed patterns of deficits in both autism and neurological patients. The performance of children with autism or orbitofrontal patients on ToM tests can be explained more parsimoniously by their deficits in lower-level domain-specific mechanisms for processing social information. Without proper inputs, the intact capacity for metarepresentation by itself cannot make correct ToM inferences. Children with autism have no impairment in false photograph tests because their metarepresentational capacity is intact and they have no impairment in inputs required for such tests. TPJ patients have equivalent deficits on ToM and non-ToM metarepresentational tasks, consistent with a failure in domain-general processing. If deficits on ToM tasks can result from deficits in low-level input systems or in higher-level domain-general capacities, postulating a separate ToM mechanism may have been an unnecessary theoretical move. C1 [Stone, Valerie E.] Univ Queensland, Sch Psychol, St Lucia, Qld 4072, Australia. [Gerrans, Philip] Univ Adelaide, Adelaide, SA, Australia. RP Stone, VE (reprint author), Univ Queensland, Sch Psychol, McElwain Bldg, St Lucia, Qld 4072, Australia. 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E., 2005, SOCIAL NEUROSCIENCE Stone VE, 1998, J COGNITIVE NEUROSCI, V10, P640, DOI 10.1162/089892998562942 STONE VE, 2006, COGNITIVE SCI, V10, P3 Suddendorf T, 2001, PSYCHOL BULL, V127, P629, DOI 10.1037//0033-2909.127.5.629 Suddendorf T, 2003, M M COG SCI, P173 Suddendorf T., 1999, DESCENT MIND PSYCHOL, P218 Wellman H. M., 1992, MIND LANG, V7, P145, DOI DOI 10.1111/J.1468-0017.1992.TB00202.X Wellman H. M., 1988, DEV THEORIES MIND, P64 Wellman HM, 2001, CHILD DEV, V72, P655, DOI 10.1111/1467-8624.00304 Wellman HM, 2000, UNDERSTANDING OTHER, P21 Wellman HM, 2004, DEVELOPMENTAL SCI, V7, P283, DOI 10.1111/j.1467-7687.2004.00347.x Woodward AL, 1999, INFANT BEHAV DEV, V22, P145, DOI 10.1016/S0163-6383(99)00007-7 NR 72 TC 57 Z9 59 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 1747-0919 J9 SOC NEUROSCI-UK JI Soc. Neurosci. PD SEP-DEC PY 2006 VL 1 IS 3-4 BP 309 EP 319 DI 10.1080/17470910601029221 PG 11 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QX UT WOS:000252245100014 PM 18633796 ER PT J AU Ashwin, C Chapman, E Colle, L Baron-Cohen, S AF Ashwin, Chris Chapman, Emma Colle, Livia Baron-Cohen, Simon TI Impaired recognition of negative basic emotions in autism: A test of the amygdala theory SO SOCIAL NEUROSCIENCE LA English DT Review ID HIGH-FUNCTIONING AUTISM; FACE PROCESSING IMPAIRMENTS; TEMPORAL-LOBE EPILEPSY; FACIAL EXPRESSIONS; ASPERGER-SYNDROME; SPECTRUM DISORDER; NORMAL ADULTS; SOCIAL INFORMATION; INFANTILE-AUTISM; BILATERAL DAMAGE AB Autism and Asperger Syndrome are autism spectrum conditions (ASC) characterized by deficits in understanding others' minds, an aspect of which involves recognizing emotional expressions. This is thought to be related to atypical function and structure of the amygdala, and performance by people with ASC on emotion recognition tasks resembles that seen in people with acquired amygdala damage. In general, emotion recognition findings in ASC have been inconsistent, which may reflect low numbers of participants, low numbers of stimuli and trials, heterogeneity of symptom severity within ASC groups, and ceiling effects on some tasks. The present study tested 39 male adults with ASC and 39 typical male controls on a task of basic emotion recognition from photographs, in two separate experiments. On a control face discrimination task the group with ASC were not impaired. People with ASC were less accurate on the emotion recognition task compared to controls, but only for the negative basic emotions. This is discussed in the light of similar findings from people with damage to the amygdala. C1 [Ashwin, Chris] Univ Essex, Dept Psychol, Colchester CO4 3SQ, Essex, England. 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PD SEP-DEC PY 2006 VL 1 IS 3-4 BP 349 EP 363 DI 10.1080/17470910601040772 PG 15 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QX UT WOS:000252245100017 PM 18633799 ER PT J AU Chakrabarti, B Bullmore, ET Baron-Cohen, S AF Chakrabarti, Bhismadev Bullmore, Edward T. Baron-Cohen, Simon TI Empathizing with basic emotions: Common and discrete neural substrates SO SOCIAL NEUROSCIENCE LA English DT Article; Proceedings Paper CT 35th Annual Meeting of the Society-for-Neuroscience CY NOV 12-16, 2005 CL Washington, DC SP Soc Neurosci ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; FACIAL EXPRESSIONS; INDIVIDUAL-DIFFERENCES; IMPAIRED RECOGNITION; PREFRONTAL CORTEX; PERMUTATION TESTS; FACE PERCEPTION; PET EXPLORATION; PREMOTOR CORTEX AB Empathizing is a quantitative trait involving understanding another's mental state (including their emotion) and responding to this with an appropriate emotion. A reliable, behaviorally validated self-report questionnaire measure of this is the Empathy Quotient (EQ), which is continuously distributed across the general population. The "discrete emotions" model posits that each "basic" emotion has a relatively independent evolutionary antecedent and social-communicative function and is subserved by a discrete neural system. In this study, we investigate if and how empathy influences the perception of basic emotions. Twenty-five volunteers (13 female, 12 male) selected across EQ space participated in a correlational design 3T fMRI study. The stimuli were presented in a box-car design, where 5 blocks (each containing 4 video clips of any one of happy, sad, angry, disgust or neutral expressions from different actors) and a low-level baseline were presented in pseudo-random order. Using an exploratory analysis, we found different brain regions correlated with EQ,depending on which emotion was being perceived. In particular, the ventral striatal response to happy faces correlated positively with EQ, while the ventral striatal response to sad faces was negatively correlated with EQ. The precuneus and lateral prefrontal cortical response to angry faces correlated positively with EQ. The response of the insula and the superior temporal gyrus cortex to disgust faces were negatively correlated with EQ. These results are discussed in the light of the postulated evolutionary function of each emotion. Using a hypothesis-driven conjunction analysis, we found that a region in the left dorsal inferior frontal gyrus/premotor cortex was positively correlated to the EQ across all four emotions. This region could therefore constitute a biomarker for trait empathy across emotions. We conclude that there are common regions underlying empathy across different emotions, and there are regions that show an emotion-specific correlation with empathy. 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Neurosci. PD SEP-DEC PY 2006 VL 1 IS 3-4 BP 364 EP 384 DI 10.1080/17470910601041317 PG 21 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QX UT WOS:000252245100018 PM 18633800 ER PT J AU Carter, EJ Pelphrey, KA AF Carter, Elizabeth J. Pelphrey, Kevin A. TI School-aged children exhibit domain-specific responses to biological motion SO SOCIAL NEUROSCIENCE LA English DT Article ID SUPERIOR TEMPORAL SULCUS; HUMAN VISUAL-CORTEX; SOCIAL-PERCEPTION; BRAIN MECHANISMS; GAIT PERCEPTION; FACE PERCEPTION; JOINT ATTENTION; HUMAN INFANTS; MIND; AUTISM AB Prior studies have implicated the superior temporal sulcus region for processing various types of biological motion in children and adults. However, no previous research in children compared this activity to that involved in coherent, meaningful, non-biological motion perception to show specificity for biological motion processing. In this study, we used functional magnetic resonance imaging to explore which brain regions were specific for biological motion in 7- to 10-year-old children. We compared brain activity in response to biological motion by a biological figure (a walking human); biological motion by a non-biological figure (a walking robot); disorganized, non-biological motion by a disjointed mechanical figure; and organized, non-biological motion by a grandfather clock. We identified a network of brain regions that had a greater response evoked by biological than by non-biological motion, including the superior temporal sulcus and mirror neuron regions. Additionally, we found a developmental change suggesting increasing specificity for biological motion with age in the superior temporal sulcus region. We discuss these results in the context of research and theory that has emphasized the important role of biological motion perception in the development of theory-of-mind abilities. 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Neurosci. PD SEP-DEC PY 2006 VL 1 IS 3-4 BP 396 EP 411 DI 10.1080/17470910601041382 PG 16 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QX UT WOS:000252245100020 PM 18174911 ER PT J AU Bernardet, M Crusio, WE AF Bernardet, Maude Crusio, Wim E. TI Fmr1 KO mice as a possible model of autistic features SO THESCIENTIFICWORLDJOURNAL LA English DT Review DE animal model; autism; autistic-like traits; behavior; Fmr1 KO mice ID FRAGILE-X-SYNDROME; MENTAL-RETARDATION PROTEIN; PERVASIVE DEVELOPMENTAL DISORDERS; UTAH EPIDEMIOLOGIC SURVEY; KNOCKOUT MICE; MOUSE MODEL; ANIMAL-MODELS; SEROTONIN TRANSPORTER; ASPERGERS-DISORDER; DENDRITIC SPINES AB Autism is a pervasive developmental disorder appearing before the age of 3, where communication and social interactions are impaired. It also entails stereotypic behavior or restricted interests. Although this disorder was first described in 1943, little is still known about its etiology and that of related developmental disorders. Work with human patients has provided many data on neuropathological and cognitive symptoms, but our understanding of the functional defects at the cellular level and how they come about remains sketchy. To improve this situation, autism research is in need of valid animal models. However, despite a strong hereditary component, attempts to identify genes have generally failed, suggesting that many different genes are involved. As a high proportion of patients suffering from the Fragile X Syndrome show many autistic symptoms, a mouse model of this disorder could potentially also serve as a model for autism. The Fmr1 KO mouse is a valid model of the Fragile X Syndrome and many data on behavioral and sensory-motor characteristics of this model have been gathered. We present here an assessment of autistic features in this candidate model. We conclude that Fmr1 KO mice display several autistic-like features, but more work is needed to validate this model. C1 Univ Bordeaux 1, CNRS, UMR 5106, Lab Neurosci Cognit, F-33405 Talence, France. RP Bernardet, M (reprint author), Univ Bordeaux 1, CNRS, UMR 5106, Lab Neurosci Cognit, Bat B2,Ave Fac, F-33405 Talence, France. 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The IDEIA requires that programs be provided in natural or least restrictive environments, and issues concerning this area have been the focus of recent litigation. In this article, the author explores the issues surrounding this litigation and offers recommendations for developing Individualized Family Service Plans (IFSPs) and Individualized Education Programs (IEPs) for young children with disabilities. An analysis of administrative and judicial decisions revealed four themes: placement decisions were based on the potential for academic and nonacademic benefits, placement decisions were based on readiness for inclusion, placement decisions were based on instructional approaches, and placement decisions must be based on the considerations of a full continuum of options. Guidelines for promoting inclusive placement decisions include expanding professional development, improving the "readiness" of inclusive placements, and coordinating the exploration of natural and inclusive environments. C1 Univ No Iowa, Cedar Falls, IA 50614 USA. RP Etscheidt, S (reprint author), Univ No Iowa, Cedar Falls, IA 50614 USA. 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Early Child. Spec. Educ. PD FAL PY 2006 VL 26 IS 3 BP 179 EP 187 DI 10.1177/02711214060260030501 PG 9 WC Education, Special SC Education & Educational Research GA 110XQ UT WOS:000242415000005 ER PT J AU Gotti, C Zoli, M Clementi, F AF Gotti, Cecilia Zoli, Michele Clementi, Francesco TI Brain nicotinic acetylcholine receptors: native subtypes and their relevance SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Review ID SUBUNIT MESSENGER-RNAS; ALPHA-CONOTOXIN-MII; CHICK OPTIC LOBE; ALZHEIMERS-DISEASE; DOPAMINE RELEASE; PARKINSONS-DISEASE; CHOLINERGIC-RECEPTORS; HETEROMERIC SUBTYPES; SUPERIOR COLLICULUS; CEREBRAL-CORTEX AB Neuronal nicotinic acetylcholine receptors comprise a heterogeneous class of cationic channels that is present throughout the nervous system. These channels are involved both in physiological functions (including cognition, reward, motor activity and analgesia) and in pathological conditions such as Alzheimer's disease, Parkinson's disease, some forms of epilepsy, depression, autism and schizophrenia. They are also the targets of tobacco-smoking effects and addiction. Neuronal nicotinic acetylcholine receptors are pentamers of homomeric or heteromeric combinations of alpha (alpha 2-alpha 10) and beta (beta 2-beta 4) subunits, which have different pharmacological and biophysical properties and locations in the brain. The lack of subtype-specific ligands and the fact that many neuronal cells express multiple subtypes initially hampered the identification of the different native nicotinic acetylcholine receptor subtypes, but the increasing knowledge of subtype composition and roles will be of considerable interest for the development of new and clinically useful nicotinic acetylcholine receptor ligands. C1 Univ Milan, CNR, Inst Neurosci Cellular & Mol Pharmacol, Dept Med Pharmacol, I-20129 Milan, Italy. Univ Milan, Ctr Excellence Neurodegenerat Dis, I-20129 Milan, Italy. Univ Modena, Dept Biomed Sci, Physiol Sect, I-41100 Modena, Italy. RP Clementi, F (reprint author), Univ Milan, CNR, Inst Neurosci Cellular & Mol Pharmacol, Dept Med Pharmacol, I-20129 Milan, Italy. 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Sci. PD SEP PY 2006 VL 27 IS 9 BP 482 EP 491 DI 10.1016/j.tips.2006.07.004 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 085NP UT WOS:000240611100006 PM 16876883 ER PT J AU Petropoulos, H Friedman, SD Shaw, DWW Artru, AA Dawson, G Dager, SR AF Petropoulos, H. Friedman, S. D. Shaw, D. W. W. Artru, A. A. Dawson, G. Dager, S. R. TI Gray matter abnormalities in autism spectrum disorder revealed by T2 relaxation SO NEUROLOGY LA English DT Article ID DIAGNOSTIC OBSERVATION SCHEDULE; WHITE-MATTER; MAGNETIC-RESONANCE; BRAIN-DEVELOPMENT; YOUNG-CHILDREN; HEAD CIRCUMFERENCE; T-2 RELAXATION; MR; VOLUME; AGE AB Objective: To perform quantitative T2 relaxation measurements to evaluate cerebral water content in children with autism. Methods: Sixty 2- to 4-year-old children with autism spectrum disorder (ASD), 16 age-matched children with idiopathic developmental delay (DD), and 10 children with typical development (TD) were scanned on a 1.5 T GE MRI scanner to obtain dual-echo fast spin echo images (2.5 mm thick, 0-mm gap). Images were segmented into gray and white matter and used to mask regions of interest for calculating T2 for each tissue type. Analysis of variance, covarying for age and sex, was used to compare T2 between groups, and correlations were used to compare T2 to IQ measures. Results: Children with ASD had prolonged cortical gray matter T2, but white matter T2 was not significantly different, compared with the children with TD. T2 was prolonged in cortical gray matter and white matter in children with DD compared with children with ASD or TD. Significant interactions between T2 measures and IQ were not observed. Conclusions: Prolonged gray and white matter T2 in the children with developmental delay likely represents a delay in neuronal development and maturation. Prolonged T2 in gray matter, but not white matter, observed in children with autism spectrum disorder may signify abnormal developmental processes specific to autism. C1 Univ Washington, Sch Med, Dept Radiol, Neuroimaging Res Grp, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Anesthesiol, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Psychol, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Psychiat, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Bioengn, Seattle, WA 98105 USA. RP Dager, SR (reprint author), Univ Washington, Sch Med, Dept Radiol, Neuroimaging Res Grp, 1100 NE 45 St,Suite 555, Seattle, WA 98105 USA. 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Structural modeling predicts an interhelical hydrophobic interface between paired EF hands in the proximal region of the Na(V)1.5COOH terminus. The predicted interface is conserved among almost all EF hand-containing proteins and is the locus of a number of disease-associated mutations. Using the structural model as a guide, we provide biochemical and biophysical evidence that the structural integrity of this interface is necessary for proper Na+ channel inactivation gating. We thus demonstrate a novel role of the sodium channel COOH terminus structure in the control of channel inactivation and in pathologies caused by inherited mutations that disrupt it. C1 Columbia Univ, Dept Pharmacol, New York, NY 10032 USA. RP Kass, RS (reprint author), Columbia Univ, Dept Pharmacol, New York, NY 10032 USA. 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Richard Ullsperger, Markus TI The control of attention and actions: Current research and future developments SO BRAIN RESEARCH LA English DT Editorial Material DE cognitive control; synopsis current issue; methods; new perspectives ID ERROR-RELATED NEGATIVITY; SOCIAL COGNITIVE NEUROSCIENCE; RESONANCE-IMAGING SIGNAL; NEURAL BASIS; FMRI SIGNAL; PERFORMANCE; DYNAMICS; AUTISM; CORTEX; BRAIN AB In this introductory article of the special issue of Brain Research, we first present an overview of some general questions relating to cognitive control. For instance, one of the questions that remain to be answered is what control mechanisms and their neural underpinnings really 'do', beyond what is done by more basic 'computational' or data processing systems in the brain. We then briefly describe the four major issues addressed in the separate articles of this issue, namely attentional orienting, task set switching, performance and error monitoring, and response inhibition. 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Mueller, Ralph-Axel TI Partially enhanced thalamocortical functional connectivity in autism SO BRAIN RESEARCH LA English DT Review DE autism; functional connectivity; thalamus; functional MRI ID PERVASIVE DEVELOPMENTAL DISORDERS; MAGNETIC-RESONANCE; SPECTRUM DISORDER; TEMPORAL-LOBE; BIOLOGICAL MOTION; HUMAN BRAIN; EMISSION-TOMOGRAPHY; SEROTONIN SYNTHESIS; CHILDHOOD AUTISM; HOME VIDEOTAPES AB Based on evidence for thalamic abnormalities in autism, impairments of thalamocortical pathways have been suspected. We examined the functional connectivity between thalamus and cerebral cortex in terms of blood oxygen level dependent (BOLD) signal cross-correlation in 8 male participants with high-functioning autism and matched normal controls, using functional MRI during simple visuomotor coordination. Both groups exhibited widespread connectivity, consistent with known extensive thalamocortical connectivity. 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PD AUG 9 PY 2006 VL 1104 BP 160 EP 174 DI 10.1016/j.brainres.2006.05.064 PG 15 WC Neurosciences SC Neurosciences & Neurology GA 082XR UT WOS:000240421000016 PM 16828063 ER PT J AU Splawski, I Yoo, DS Stotz, SC Cherry, A Clapham, DE Keating, MT AF Splawski, Igor Yoo, Dana S. Stotz, Stephanie C. Cherry, Allison Clapham, David E. Keating, Mark T. TI CACNA1H mutations in autism spectrum disorders SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDHOOD ABSENCE EPILEPSY; CALCIUM-CHANNELS AB Autism spectrum disorders (ASD) are neurodevelopmental conditions characterized by impaired social interaction, communication skills, and restricted and repetitive behavior. The genetic causes for autism are largely unknown. Previous studies implicate CACNA1C (L-type Ca(V)1.2) calcium channel mutations in a disorder associated with autism (Timothy syndrome). Here, we identify missense mutations in the calcium channel gene CACNA1H (T-type Ca(V)3.2) in 6 of 461 individuals with ASD. These mutations are located in conserved and functionally relevant domains and are absent in 480 ethnically matched controls (p = 0.014, Fisher's exact test). Non-segregation within the pedigrees between the mutations and the ASD phenotype clearly suggest that the mutations alone are not responsible for the condition. However, functional analysis shows that all these mutations significantly reduce CaV3.2 channel activity and thus could affect neuronal function and potentially brain development. We conclude that the identified mutations could contribute to the development of the ASD phenotype. C1 Childrens Hosp, Dept Cardiol, Howard Hughes Med Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA. RP Stotz, SC (reprint author), Childrens Hosp, Dept Cardiol, Howard Hughes Med Inst, Enders 1314,320 Longwood Ave, Boston, MA 02115 USA. EM scstotz@enders.tch.harvard.edu CR Brambilla P, 2003, BRAIN RES BULL, V61, P557, DOI 10.1016/j.brainresbull.2003.06.001 Bryson SE, 2003, CAN J PSYCHIAT, V48, P506 Chemin J, 2000, FEBS LETT, V478, P166, DOI 10.1016/S0014-5793(00)01832-9 Chen YC, 2003, ANN NEUROL, V54, P239, DOI 10.1002/ana.10607 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Geschwind DH, 2001, AM J HUM GENET, V69, P463, DOI 10.1086/321292 Hille B, 2001, ION CHANNELS EXCITAB JOKSOVIC P, 2006, IN PRESS J PHYSL Khosravani H, 2005, ANN NEUROL, V57, P745, DOI 10.1002/ana.20458 KHOSRAVANI H, 2004, J BIOL CHEM, V279, P2681 Long SB, 2005, SCIENCE, V309, P903, DOI 10.1126/science.1116270 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 McCormick DA, 1997, ANNU REV NEUROSCI, V20, P185, DOI 10.1146/annurev.neuro.20.1.185 Muhle R., 2004, PEDIATRICS, V113, P472 Perez-Reyes E, 2003, PHYSIOL REV, V83, P117, DOI 10.1152/physrev.00018.2002 Sadamatsu Miyuki, 2006, Congenital Anomalies, V46, P1, DOI 10.1111/j.1741-4520.2006.00094.x Splawski I., 2005, P NATL ACAD SCI USA, V102, P8086, DOI [10.1073/pnas.0502506102, DOI 10.1073/PNAS.050250] Splawski I, 2004, CELL, V119, P19, DOI 10.1016/j.cell.2004.09.011 Splawski I, 1997, NAT GENET, V17, P338, DOI 10.1038/ng1197-338 Talley EM, 1999, J NEUROSCI, V19, P1895 Vitko I, 2005, J NEUROSCI, V25, P4844, DOI 10.1523/JNEUROSCI.0847-05.2005 Volkmar FR, 2003, LANCET, V362, P1133, DOI 10.1016/S0140-6736(03)14471-6 Weiss LA, 2003, MOL PSYCHIATR, V8, P186, DOI 10.1038/sj.mp.4001241 Zhong XL, 2006, HUM MOL GENET, V15, P1497, DOI 10.1093/hmg/ddl068 Zoghbi HY, 2003, SCIENCE, V302, P826, DOI 10.1126/science.1089071 NR 26 TC 77 Z9 84 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 4 PY 2006 VL 281 IS 31 BP 22085 EP 22091 DI 10.1074/jbc.M603316200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 068PO UT WOS:000239387100055 PM 16754686 ER PT J AU Silk, TJ Rinehart, N Bradshaw, JL Tonge, B Egan, G O'Boyle, MW Cunnington, R AF Silk, Timothy J. Rinehart, Nicole Bradshaw, John L. Tonge, Bruce Egan, Gary O'Boyle, Michael W. Cunnington, Ross TI Visuospatial processing and the function of prefrontal-parietal networks in autism spectrum disorders: a functional MRI study SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article AB Objective: Individuals with autism spectrum disorders typically have normal visuospatial abilities but impaired executive functioning, particularly in abilities related to working memory and attention. The aim of this study was to elucidate the functioning of frontoparietal networks underlying spatial working memory processes during mental rotation in persons with autism spectrum disorders. Method: Seven adolescent males with normal IQ with an autism spectrum disorder and nine age- and IQ-matched male comparison subjects underwent functional magnetic resonance imaging scans while performing a mental rotation task. Results: The autism spectrum disorders group showed less activation in lateral and medial premotor cortex, dorsolateral prefrontal cortex, anterior cingulate gyrus, and caudate nucleus. Conclusions: The finding of less activation in prefrontal regions but not in parietal regions supports a model of dysfunction of frontostriatal networks in autism spectrum disorders. C1 Univ Melbourne, Howard Florey Inst, Melbourne, Vic 3010, Australia. RP Cunnington, R (reprint author), Univ Melbourne, Howard Florey Inst, Melbourne, Vic 3010, Australia. EM r.cunnington@hfi.unimelb.edu.au RI Cunnington, Ross/C-8432-2009; Egan, Gary/A-1381-2013 CR Achenbach TM, 1991, MANUAL CHILD BEHAV C Caron MJ, 2004, NEUROPSYCHOLOGIA, V42, P467, DOI 10.1016/j.neuropsychologia.2003.08.015 Cohen MS, 1996, BRAIN, V119, P89, DOI 10.1093/brain/119.1.89 Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Luna B, 2002, NEUROLOGY, V59, P834 Ohnishi T, 2000, BRAIN, V123, P1838, DOI 10.1093/brain/123.9.1838 Piven J, 1996, J AM ACAD CHILD PSY, V35, P530, DOI 10.1097/00004583-199604000-00020 Rinehart NJ, 2002, AUST NZ J PSYCHIAT, V36, P762, DOI 10.1046/j.1440-1614.2002.01097.x Russell J., 1997, AUTISM EXECUTIVE DIS Sakata H, 1997, TRENDS NEUROSCI, V20, P350, DOI 10.1016/S0166-2236(97)01067-9 Silk T, 2005, BRIT J PSYCHIAT, V187, P282, DOI 10.1192/bjp.187.3.282 NR 12 TC 66 Z9 66 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD AUG PY 2006 VL 163 IS 8 BP 1440 EP U3 DI 10.1176/appi.ajp.163.8.1440 PG 4 WC Psychiatry SC Psychiatry GA 068FT UT WOS:000239358800026 PM 16877661 ER PT J AU Yao, YM Walsh, WJ McGinnis, WR Pratico, D AF Yao, Yuemang Walsh, William J. McGinnis, Woody R. Pratico, Domenico TI Altered vascular phenotype in autism: Correlation with oxidative stress SO ARCHIVES OF NEUROLOGY LA English DT Article ID LIPID-PEROXIDATION; CHILDREN; ENZYMES; MODELS AB Background: Autism is a neurologic disorder characterized by impaired communication and social interaction. Results of previous studies showed biochemical evidence for abnormal platelet reactivity and altered blood flow in children with autism. Objective: To evaluate the vascular phenotype in children with autism. Design and Main outcome Measures: Urinary levels of isoprostane F-2 alpha-VI, a marker of lipid peroxidation; 2,3-dinor-thromboxane B-2, which reflects platelet activation; and 6-keto-prostaglandin F-1 alpha, a marker of endothelium activation, were measured by means of gas chromatography-mass spectrometry in subjects with autism and healthy control subjects. Setting and Subjects: Children with a clinical diagnosis of autism attending the Pfeiffer Treatment Center. Results: Compared with controls, children with autism had significantly higher urinary levels of isoprostane F-2 alpha-VI, 2,3-dinor-thromboxane B2, and 6-ketoprostaglandin F-1 alpha. Lipid peroxidation levels directly correlated with both vascular biomarker ratios. Conclusion: Besides enhanced oxidative stress, platelet and vascular endothelium activation also could contribute to the development and clinical manifestations of autism. C1 Univ Penn, Sch Med, Dept Pharmacol, Philadelphia, PA 19104 USA. Pfeiffer Treatment Ctr, Warrenville, IL USA. RP Pratico, D (reprint author), Univ Penn, Sch Med, Dept Pharmacol, 3620 Hamilton Walk,John Morgan Bldg,Room 124, Philadelphia, PA 19104 USA. 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Neurol. PD AUG PY 2006 VL 63 IS 8 BP 1161 EP 1164 DI 10.1001/archneur.63.8.1161 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 072ER UT WOS:000239656400018 PM 16908745 ER PT J AU Gurney, JG McPheeters, ML Davis, MM AF Gurney, James G. McPheeters, Melissa L. Davis, Matthew M. TI Parental report of health conditions and health care use among children with and without autism - National Survey of Children's Health SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID SPECTRUM DISORDERS; GASTROINTESTINAL DISORDERS; TUBEROUS SCLEROSIS; MEDICAL CONDITIONS; PREVALENCE TRENDS; ASPERGER-SYNDROME; ABNORMALITIES; EPILEPSY; DISABILITIES; INDIVIDUALS AB Objective: To compare parent-reported prevalence of health conditions and health care use between children with and without autism. Design: Cross-sectional analysis of the 2003 to 2004 National Survey of Children's Health. Setting: Population-based sample across the United States. Participants: More than 100 000 parents. The main exposure was "autism" (not further defined), from response to the question: "Has a doctor or health professional ever told you that your child has autism?" Main Outcome Measures: Medical and mental health conditions and measures of health care use. Results: Autism prevalence among children aged 3 to 17 years was 53 per 10 000 (95% confidence interval, 45-61 per 10 000), equating to a national estimate of 324 000 children (95% confidence interval, 274 000-375 000 children). Children with autism had a significantly (P <.001) higher prevalence of depression or anxiety problems (38.9% vs 4.2%) and behavioral or conduct problems (58.9% vs 5.2%) than children without autism. Respiratory, food, and skin allergies were reported by parents more often for children with autism, with food allergies having the strongest relative difference between the groups (odds ratio, 4.5; 95% confidence interval, 3.0-7.0). Children with autism had significantly (P <.001) higher mean physician visits over 12 months for preventive care, nonemergency care, and hospital emergency care, and were far more likely than children without autism to receive physical, occupational, or speech therapy (76.0% vs 6.3%), to need treatment or counseling for an emotional, developmental, or behavioral problem (75.4% vs 7.0%), and, among those taking a prescribed medication, to be using a medication long-term (51.4% vs 14.5%). Conclusion: We found markedly higher reports of concurrent conditions and health care use associated with childhood autism in this study. C1 Univ Michigan, Dept Pediat, Child Hlth Evaluat & Res Unit, Ann Arbor, MI 48109 USA. Univ Michigan, Gerald R Ford Sch Publ Policy, Div Gen Internal Med, Ann Arbor, MI 48109 USA. RP Gurney, JG (reprint author), Univ Michigan, Dept Pediat, Child Hlth Evaluat & Res Unit, 300 N Ingalls St,Room 6E02, Ann Arbor, MI 48109 USA. 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Pediatr. Adolesc. Med. PD AUG PY 2006 VL 160 IS 8 BP 825 EP 830 DI 10.1001/archpedi.160.8.825 PG 6 WC Pediatrics SC Pediatrics GA 071BX UT WOS:000239573400010 PM 16894082 ER PT J AU Gernsbacher, MA Dawson, M Mottron, L AF Gernsbacher, Morton Ann Dawson, Michelle Mottron, Laurent TI Autism: Common, heritable, but not harmful SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID CHILDREN AB We assert that one of the examples used by Keller & Miller (K&M), namely, autism, is indeed common, and heritable, but we question whether it is harmful. We provide a brief review of cognitive science literature in which autistics perform superiorly to non-autistics in perceptual, reasoning, and comprehension tasks; however, these superiorities are often occluded and are instead described as dysfunctions. C1 Univ Wisconsin, Dept Psychol, Madison, WI 53706 USA. Univ Montreal, Pervas Dev Disorders Specialized Clin, Montreal, PQ H1E 1A4, Canada. RP Gernsbacher, MA (reprint author), Univ Wisconsin, Dept Psychol, 1202 W Johnson St, Madison, WI 53706 USA. 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TI Mapping corpus callosum deficits in autism: An index of aberrant cortical connectivity SO BIOLOGICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT 11th Annual Meeting of the International-Society-for-Magnetic-Resonance-in-Medicine CY JUL 10-16, 2003 CL TORONTO, CANADA SP Int Soc Magnet Resonance Med DE autism; corpus callosum; imaging; MRI; three-dimensional (3D) maps; white matter ID RHESUS-MONKEY; PREFRONTAL CORTEX; SPECTRUM DISORDER; BRAIN STRUCTURE; SIZE; INDIVIDUALS; SCHIZOPHRENIA; ABNORMALITIES; MORPHOMETRY; TOPOGRAPHY AB Background: Volumetric studies have reported reductions in the size of the corpus callosum (CC) in autism, but the callosal regions contributing to this deficit have differed among studies. In this study, a computational method was used to detect and map the spatial pattern of CC abnormalities in mate patients with autism. Methods. Twenty-four boys with autism (aged 10.0 +/- 3.3 years) and 26 control boys (aged 11.0 +/- 2.5 years) underwent a magnetic resonance imaging WRO scan at 3 Tesla. Total and regional areas of the CC were determined using traditional morphometric methods. Three-dimensional (3D) surface models of the CC were also created from the MRI scans. Statistical maps were created to visualize morphologic variability of the CC and to localize regions of callosal thinning in autism. Results. Traditional morphometric methods detected a significant reduction in the total callosal area and in the anterior third of the CC inpatients with autism; however, 3D maps revealed significant reductions in both the splenium and genu of the CC inpatients. Conclusions: Statistical maps of the CC revealed callosal deficits in autism with greater precision than traditional morphometric methods. 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We compared inattentive, hyperactive, and impulsive (IHI) behaviours in the 2 groups, along with adaptive functioning and medical circumstances. We further subdivided the autism group into those with IHI behaviours (autism IHI) and those without (autism non-IHI) and explored similarities and differences between autism subgroups. Results: As a group, those with autism and ID had more IHI behaviours than those with ID alone. More in the autism group met criteria for attention-deficit hyperactivity disorder and hyperkinetic syndrome. Lifetime exposure to psychotropic medication was greater in the autism group, with stimulant and antipsychotic medications predominating. However, just under one-half of those in the autism group showed no IHI behaviours. Comparison of autism IHI and autism non-IHI groups showed that those with IHI behaviours were significantly more likely to have past (but not current) exposure to stimulant medication. 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PD AUG PY 2006 VL 12 IS 4-5 BP 245 EP 246 DI 10.1080/09297040600788128 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000001 ER PT J AU Bishop, SL Richler, J Lord, C AF Bishop, Somer L. Richler, Jennifer Lord, Catherine TI Association between restricted and repetitive behaviors and nonverbal IQ in children with autism spectrum disorders SO CHILD NEUROPSYCHOLOGY LA English DT Article DE Autism Spectrum Disorders; restricted and repetitive behaviors; nonverbal IQ ID DIFFERENTIAL ABILITY SCALES; ASPERGER-SYNDROME; FOLLOW-UP; LEARNING-DISABILITIES; DIAGNOSTIC INTERVIEW; CLINICAL-FEATURES; ADULTS; AGE AB The present study explored the relationship between nonverbal IQ and restricted and repetitive behaviors (RRBs) in 830 children with Autism Spectrum Disorders. The role of chronological age as a moderator of this relationship was also investigated. For many behaviors, there was a significant interaction between nonverbal IQ and chronological age, such that nonverbal IQ (NVIQ) was more strongly related to the prevalence of RRBs in older children. For the majority of such behaviors (e.g. repetitive use of objects, hand and finger mannerisms), RRB prevalence was negatively associated with NVIQ. However, the prevalence of certain behaviors (e.g. circumscribed interests) showed positive relationships with NVIQ, which provides some support for the idea of different classes of RRBs. For the severity of different RRBs, there were several significant effects for age and NVIQ, but few interactions. C1 Univ Michigan, Autism & Commun Disorders Ctr, UMACC, Ann Arbor, MI 48109 USA. RP Bishop, SL (reprint author), Univ Michigan, Autism & Commun Disorders Ctr, UMACC, 1111 E Catherine St, Ann Arbor, MI 48109 USA. 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PD AUG PY 2006 VL 12 IS 4-5 BP 247 EP 267 DI 10.1080/09297040600630288 PG 21 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000002 PM 16911971 ER PT J AU Akshoomoff, N AF Akshoomoff, Natacha TI Use of the mullen scales of early learning for the assessment of young children with autism spectrum disorders SO CHILD NEUROPSYCHOLOGY LA English DT Article ID DEVELOPMENTAL DISORDERS; PRESCHOOL-CHILDREN; HOME VIDEOTAPES; AGE; RECOGNITION; CAREGIVERS; DIAGNOSIS; 1ST AB The psychological assessment is an important component of the diagnostic evaluation in young children suspected of having an Autism Spectrum Disorder but can be hampered by behavioral difficulties. Overt behaviors during administration of the Mullen Scales of Early Learning were coded in 22 preschoolers with an Autism Spectrum Disorder and 20 age-matched typically developing children. 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PD AUG PY 2006 VL 12 IS 4-5 BP 269 EP 277 DI 10.1080/09297040500473714 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000003 PM 16911972 ER PT J AU Williams, DL Goldstein, G Minshew, NJ AF Williams, Diane L. Goldstein, Gerald Minshew, Nancy J. TI Neuropsychologic functioning in children with autism: Further evidence for disordered complex information-processing SO CHILD NEUROPSYCHOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; IMPAIRED MEMORY FUNCTIONS; NEOCORTICAL SYSTEMS; EXECUTIVE FUNCTIONS; SPECTRUM DISORDERS; INFANTILE-AUTISM; JOINT ATTENTION; INDIVIDUALS; PERFORMANCE AB A wide range of abilities was assessed in 56 high-functioning children with autism and 56 age- and IQ-matched controls. Stepwise discriminant analyses produced good group discrimination for sensory-perceptual, motor, complex language, and complex memory domains but lower agreement for the reasoning domain than previously obtained for adults. Group discrimination did not occur for attention, simple language, simple memory, and visuospatial domains. Findings provide additional support for a complex information-processing model for autism, previously based on adult data, demonstrating a pattern across domains of selective impairments on measures with high demands for integration of information and sparing when demands were low. Children as compared to adults with autism exhibited more prominent sensory-perceptual symptoms and less pronounced reasoning deficits reflecting brain maturation. C1 Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA. VA PIttsburgh Healthcare Syst, Pittsburgh, PA USA. RP Minshew, NJ (reprint author), Webster Hall,Suite 300,3811 OHara St, Pittsburgh, PA 15213 USA. 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S., 1993, WIDE RANGE ACHIEVEME Woodcock R., 1987, WOODCOCK READING MAS Zwaigenbaum L, 2005, INT J DEV NEUROSCI, V23, P143, DOI 10.1016/j.ijdevneu.2004.05.001 NR 97 TC 69 Z9 70 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0929-7049 J9 CHILD NEUROPSYCHOL JI Child Neuropsychol. PD AUG PY 2006 VL 12 IS 4-5 BP 279 EP 298 DI 10.1080/09297040600681190 PG 20 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000004 PM 16911973 ER PT J AU Hooper, SR Poon, KK Marcus, L Fine, C AF Hooper, Stephen R. Poon, Kenneth K. Marcus, Lee Fine, Camille TI Neuropsychological characteristics of school-age children with high-functioning autism: Performance on the NEPSY SO CHILD NEUROPSYCHOLOGY LA English DT Article ID DISORDERS; LANGUAGE; MEMORY AB Utilizing standardization and validation data from the NEPSY, this study presents a reanalysis of the High-Functioning Autism (HFA) versus Typical samples using IQ as a covariate. The reanalysis in the present paper should prove important to clinicians and researchers by (1) determining if the original findings can be replicated for the HFA sample when controlling for IQ, and (2) providing neuropsychological description for children with HFA versus Typical children across the NEPSY variables. The sample included 23 children with HFA who ranged in age from 5 years 5 months to 12 years 11 months (Mean = 9.59 years). The HFA Group comprised 19 males, 22 Caucasians, and was 87% right handed. All of the parents had between 12 to 15 years of education. A Typical Group was selected from the standardization sample of the NEPSY and matched on the variables of chronological age, race, gender, parental education, and region of the country. A MANCOVA revealed significant group differences on 8 of the 14 core subtests of the NEPSY, with the HFA Group performing lower than the Typical Group. While these findings significantly overlapped with those from the original validation study, significant group differences also were uncovered for the subtests of Phonological Processing, Auditory Attention and Response Set, and Speeded Naming; Comprehension of Instructions and Narrative Memory were no longer significant after controlling for IQ. When the groups were compared with respect to the number of cases falling below the 10(th) percentile, the HFA Group showed a higher rate of occurrence on each subtest, but only significantly so on the Arrows Subtest. These findings provide additional support for the phenotypic neurocognitive presentation of individuals with HFA, and they suggest that the NEPSY can contribute to the neuropsychological description of children with HFA. C1 Univ N Carolina, Sch Med, Ctr Dev & Learning, Dept Psychiat, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Med, Clin Ctr Study Dev & Learning, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Educ, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Med, Div TEACCH, Chapel Hill, NC 27599 USA. NeuroDev Solut, Parrish, FL USA. RP Hooper, SR (reprint author), Univ N Carolina, Sch Med, Ctr Dev & Learning, Dept Psychiat, CB 7255, Chapel Hill, NC 27599 USA. EM stephen.hooper@cdl.unc.edu RI Poon, Kenneth /K-5799-2012 OI Poon, Kenneth /0000-0002-8809-902X CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baranek G., 2005, HDB AUTISM PERVASIVE, V2 Frith U., 2003, AUTISM EXPLAINING EN Ghaziuddin M, 2004, J AUTISM DEV DISORD, V34, P279, DOI 10.1023/B:JADD.0000029550.19098.77 Gillberg C., 1992, BIOL AUTISTIC SYNDRO Hauck M, 1998, CHILD NEUROPSYCHOL, V4, P187, DOI 10.1076/chin.4.3.187.3174 Korkman M., 1998, NEPSY DEV NEUROPSYCH Liss M, 2001, J CHILD PSYCHOL PSYC, V42, P261, DOI 10.1017/S0021963001006679 LURIA AR, 1966, WORKING BRAIN MINSHEW NJ, 1995, NEUROPSYCHOLOGY, V9, P255, DOI 10.1037//0894-4105.9.2.255 Minshew NJ, 2001, J CHILD PSYCHOL PSYC, V42, P1095, DOI 10.1111/1469-7610.00808 Ozonoff S, 1997, J AUTISM DEV DISORD, V27, P59, DOI 10.1023/A:1025821222046 Ozonoff S, 2004, J AUTISM DEV DISORD, V34, P139, DOI 10.1023/B:JADD.0000022605.81989.cc Ozonoff S, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Rinehart NJ, 2001, J AUTISM DEV DISORD, V31, P79, DOI 10.1023/A:1005617831035 Sattler J. M, 2004, ASSESSMENT CHILDREN Starr E, 2003, J AUTISM DEV DISORD, V33, P15, DOI 10.1023/A:1022222202970 Tager-Flusberg H, 2004, J AUTISM DEV DISORD, V34, P75, DOI 10.1023/B:JADD.0000018077.64617.5a Tsatsanis K., 2005, HDB AUTISM PERVASIVE, V1, P365 NR 19 TC 12 Z9 12 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0929-7049 J9 CHILD NEUROPSYCHOL JI Child Neuropsychol. PD AUG PY 2006 VL 12 IS 4-5 BP 299 EP 305 DI 10.1080/09297040600737984 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000005 PM 16911974 ER PT J AU Colgan, SE Lanter, E McComish, C Watson, LR Crais, ER Baranek, GT AF Colgan, Siobhan E. Lanter, Elizabeth McComish, Cara Watson, Linda R. Crais, Elizabeth R. Baranek, Grace T. TI Analysis of social interaction gestures in infants with autism SO CHILD NEUROPSYCHOLOGY LA English DT Article ID RETROSPECTIVE VIDEO ANALYSIS; LANGUAGE-DEVELOPMENT; MENTAL-RETARDATION; SPECTRUM DISORDER; EARLY RECOGNITION; JOINT ATTENTION; YOUNG-CHILDREN; DELAY; LIFE; 1ST AB This study analyzes the emergent use of gestures used among 9-12-month-old infants with autism and typical development using retrospective video analysis. The purpose of the present investigation was to examine the frequency, initiation, prompting, and diversity of types of gestures used for social interaction purposes. It was hypothesized that a restricted variety in type(s) of gestures as well as fewer child-initiated gestures and more prompted gestures would be associated with later diagnosis of autism. Logistic regression analysis found that decreased variety in type of gestures used was significantly associated with autism status. Neither number of total gestures nor initiation of gestures (child-initiated vs. prompted) was significantly associated with autism status. C1 Univ N Carolina, Sch Educ, Chapel Hill, NC 27599 USA. RP Colgan, SE (reprint author), Univ N Carolina, Sch Educ, CB 3500,Peabody Hall, Chapel Hill, NC 27599 USA. 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PD AUG PY 2006 VL 12 IS 4-5 BP 307 EP 319 DI 10.1080/09297040600701360 PG 13 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000006 PM 16911975 ER PT J AU Pearson, DA Loveland, KA Lachar, D Lane, DM Reddoch, SL Mansour, R Cleveland, LA AF Pearson, Deborah A. Loveland, Katherine A. Lachar, David Lane, David M. Reddoch, Stacy L. Mansour, Rosleen Cleveland, Lynne A. TI A comparison of behavioral and emotional functioning in children and adolescents with autistic disorder and PDD-NOS SO CHILD NEUROPSYCHOLOGY LA English DT Article; Proceedings Paper CT 4th International Meeting for Autism Research CY MAY 06-07, 2005 CL Boston, MA ID PERVASIVE DEVELOPMENTAL DISORDERS; PERSONALITY-INVENTORY; PSYCHIATRIC-DISORDERS; PRESCHOOL-CHILDREN; ASPERGER-SYNDROME; SYMPTOMS; DEPRESSION; PATTERNS AB Behavioral symptomatology was compared in 26 children and adolescents with Autistic Disorder ("autism") and 25 children and adolescents with Pervasive Developmental Disorder, Not Otherwise Specified ("PDD-NOS"). Relative to individuals with PDD-NOS, those with autism had more symptoms of depression, social withdrawal, atypical behavior, and immature social skills-and fewer family problems. These differences remained even when group differences in intellectual ability were statistically controlled. No group differences emerged in somatization, anxiety, or hyperactivity. 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T., 2000, ASPERGER SYNDROME, P172 STEWART SL, 1995, DEV PSYCHOPATHOL, V7, P323 Sturm H, 2004, DEV MED CHILD NEUROL, V46, P444, DOI 10.1017/S0012162204000738 Sverd Jeffrey, 2003, J Psychiatr Pract, V9, P111, DOI 10.1097/00131746-200303000-00003 Thorndike RL, 1986, STANFORD BINET INTEL Tsai LY, 1996, J AUTISM DEV DISORD, V26, P159, DOI 10.1007/BF02172004 Valente S., 2004, J AM PSYCHIAT NURSES, V10, P236, DOI 10.1177/1078390304269789 Wechsler D., 1989, WECHSLER PRESCHOOL P Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WIRT RD, 1984, MULTIDIMENSIONAL DES NR 61 TC 30 Z9 30 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0929-7049 J9 CHILD NEUROPSYCHOL JI Child Neuropsychol. PD AUG PY 2006 VL 12 IS 4-5 BP 321 EP 333 DI 10.1080/092970406006464847 PG 13 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000007 PM 16911976 ER PT J AU Corbett, BA Constantine, LJ AF Corbett, Blythe A. Constantine, Laura J. TI Autism and attention deficit hyperactivity disorder: Assessing attention and response control with the Integrated Visual and Auditory Continuous Performance Test SO CHILD NEUROPSYCHOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDER; ABNORMAL-PSYCHICAL-CONDITIONS; DEFICIT/HYPERACTIVITY DISORDER; DIFFERENTIAL-DIAGNOSIS; GOULSTONIAN-LECTURES; SPECTRUM DISORDER; CHILDREN; ADHD; COMORBIDITY; PDD AB Symptoms of attention deficit hyperactivity disorder (ADHD) have been widely reported in children with autism spectrum disorder (ASD). The current study investigated attention and response control in children with ASD, ADHD, and typical development using the Integrated Visual and Auditory Continuous Performance Test. Results indicate that many children with ASD show significant deficits in visual and auditory attention and greater deficits in impulsivity than children with ADHD or typical development. These findings suggest that many of the children with ASD demonstrate significant ADHD-like deficits. These findings are discussed in the context of symptoms, subtypes, and comorbidity. C1 Univ Calif Davis, Dept Psychiat & Behav Sci, MIND Inst, Sacramento, CA 95817 USA. RP Corbett, BA (reprint author), Univ Calif Davis, Dept Psychiat & Behav Sci, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. EM blythe.corbett@ucdmc.ucdavis.edu CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th Barkley RA, 1990, ATTENTION DEFICIT HY, V2nd BARKLEY RA, 1994, ADHD REPORT, V1, P1 Barkley RA, 1993, ADHD REPORT, V1, P1 Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 Bonde E, 2000, EUR CHILD ADOLES PSY, V9, P7 Brewis A, 2002, SOC BIOL, V49, P99 Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Clark T, 1999, EUR CHILD ADOLES PSY, V8, P50 Conners K., 2001, CONNERS RATING SCALE COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 COURCHESNE E, 1989, J AUTISM DEV DISORD, V19, P1, DOI 10.1007/BF02212714 DAWSON G, 1989, BRAIN LANG, V37, P26, DOI 10.1016/0093-934X(89)90099-0 DUPAUL GJ, 1992, J CLIN CHILD PSYCHOL, V21, P394, DOI 10.1207/s15374424jccp2104_10 Frazier J. 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A., 2000, INTEGRATED VISUAL AU Shaffer D, 1996, J AM ACAD CHILD PSY, V35, P865, DOI 10.1097/00004583-199607000-00012 SIEGEL BV, 1995, SCHIZOPHR RES, V17, P85, DOI 10.1016/0920-9964(95)00033-I Spreen O., 1998, COMPENDIUM NEUROPSYC Still GF, 1902, LANCET, V1, P1163 Still GF, 1902, LANCET, V1, P1008 STRANDBURG RJ, 1993, NEUROPSYCHOLOGIA, V31, P413, DOI 10.1016/0028-3932(93)90058-8 Sturm H, 2004, DEV MED CHILD NEUROL, V46, P444, DOI 10.1017/S0012162204000738 Tinius TP, 2003, ARCH CLIN NEUROPSYCH, V18, P439, DOI 10.1016/S0887-6177(02)00144-0 WAINWRIGHTSHARP JA, 1993, J AUTISM DEV DISORD, V23, P1, DOI 10.1007/BF01066415 Wechsler D, 1999, WECHSLER ABBREVIATED Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 Yoshida Y, 2004, EUR CHILD ADOLES PSY, V13, P307, DOI 10.1007/s00787-004-0391-1 NR 53 TC 47 Z9 51 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0929-7049 J9 CHILD NEUROPSYCHOL JI Child Neuropsychol. PD AUG PY 2006 VL 12 IS 4-5 BP 335 EP 348 DI 10.1080/09297040500350938 PG 14 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000008 PM 16911977 ER PT J AU Raymaekers, R van der Meere, J Roeyers, H AF Raymaekers, Ruth van der Meere, Jaap Roeyers, Herbert TI Response inhibition and immediate arousal in children with high-functioning autism SO CHILD NEUROPSYCHOLOGY LA English DT Article DE HFA; response inhibition; arousal regulation ID EXECUTIVE FUNCTIONS; STIMULUS-INTENSITY; ASPERGER-SYNDROME; TOURETTE-SYNDROME; DISORDERS; ADULTS; PERFORMANCE; TIME; INDIVIDUALS; DYSFUNCTION AB The current study compared high-functioning children with autism (HFA) and a peer control group on an immediate arousal task measuring response inhibition. In one condition go stimuli were presented whereas in another condition a tone preceded the go stimulus. The tone caused an immediate arousal effect, which resulted in a reaction time decrease and an error rate increase. It was expected that children with HFA would produce a higher error rate in comparison with normal peers, since they might be less able to suppress immediate arousal. However, the HFA group outperformed the control group, indicating neither arousal regulation deficit nor response inhibition deficit. C1 Univ Ghent, Ghent, Belgium. Univ Groningen, NL-9700 AB Groningen, Netherlands. RP Raymaekers, R (reprint author), Res Grp Dev Disorders, Dept Expt Clin & Hlth Psychol, Dunantlaan 2, B-9000 Ghent, Belgium. EM Ruth.Raymaekers@UGent.be CR Achenbach T. 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C., 1996, HANDLEIDING VOOR CBC VERHULST FC, 1997, HANDLEIDING VOOR TRF Verte S, 2005, DEV PSYCHOPATHOL, V17, P415, DOI 10.1017/S0954579405050200 Warreyn P, 2004, VRAGENLIJST SOCIALE Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WELSH MC, 1988, DEV NEUROPSYCHOL, V4, P199 NR 54 TC 6 Z9 6 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0929-7049 J9 CHILD NEUROPSYCHOL JI Child Neuropsychol. PD AUG PY 2006 VL 12 IS 4-5 BP 349 EP 359 DI 10.1080/09297040600760457 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000009 PM 16911978 ER PT J AU Renner, P Klinger, LG Klinger, MR AF Renner, Peggy Klinger, Laura Grofer Klinger, Mark R. TI Exogenous and endogenous attention orienting in Autism Spectrum Disorders SO CHILD NEUROPSYCHOLOGY LA English DT Article ID VISUAL-ATTENTION; SELECTIVE ATTENTION; SPATIAL ATTENTION; EARLY RECOGNITION; JOINT ATTENTION; PERIPHERAL CUES; TIME-COURSE; CHILDREN; DEFICITS; ABNORMALITY AB Fifteen children with high-functioning Autism Spectrum Disorder (ASD) and 15 children with typical development completed an attentional cuing task using peripheral cues (exogenous orienting) and central cues (endogenous orienting). Results showed that participants with ASD had impaired exogenous and intact endogenous orienting. The pattern of exogenous orienting was related to motor functioning. Individuals with ASD who had poor motor functioning displayed slowed exogenous orienting. However, individuals with ASD who had relatively good motor functioning showed typical levels of exogenous orienting when given a short time but decreased orienting when given a longer amount of time. These results suggest attention impairments in ASD may not be specific to social orienting and instead may represent a more general orienting impairment. C1 Univ Alabama, Dept Psychol, Tuscaloosa, AL 35487 USA. RP Klinger, LG (reprint author), Univ Alabama, Dept Psychol, Box 870348, Tuscaloosa, AL 35487 USA. EM lklinger@bama.ua.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ATKINSON J, 1992, PERCEPTION, V21, P643, DOI 10.1068/p210643 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 Belmonte MK, 2003, COGNITIVE BRAIN RES, V17, P651, DOI 10.1016/S0926-6410(03)00189-7 Brodeur D., 1997, ATTENTION DEV PSYCHO, P74 Casey B. 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A, 1996, ATTENTION EARLY DEV RUTTER M, 2003, AUTISM DIAGNOSTIC IN Senju A, 2004, J CHILD PSYCHOL PSYC, V45, P445, DOI 10.1111/j.1469-7610.2004.00236.x SHEPHERD M, 1989, PERCEPT PSYCHOPHYS, V46, P146, DOI 10.3758/BF03204974 SPENCE CJ, 1994, J EXP PSYCHOL HUMAN, V20, P555, DOI 10.1037//0096-1523.20.3.555 THEEUWES J, 1991, PERCEPT PSYCHOPHYS, V49, P83, DOI 10.3758/BF03211619 Townsend J, 1999, J NEUROSCI, V19, P5632 Townsend J, 1996, J Int Neuropsychol Soc, V2, P541 Townsend J, 1996, DEV PSYCHOPATHOL, V8, P563 Wainwright JA, 1996, J AUTISM DEV DISORD, V26, P423, DOI 10.1007/BF02172827 WAINWRIGHTSHARP JA, 1993, J AUTISM DEV DISORD, V23, P1, DOI 10.1007/BF01066415 YANTIS S, 1990, J EXP PSYCHOL HUMAN, V16, P121, DOI 10.1037//0096-1523.16.1.121 NR 55 TC 22 Z9 23 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0929-7049 J9 CHILD NEUROPSYCHOL JI Child Neuropsychol. PD AUG PY 2006 VL 12 IS 4-5 BP 361 EP 382 DI 10.1080/09297040600770753 PG 22 WC Clinical Neurology SC Neurosciences & Neurology GA 073UL UT WOS:000239768000010 PM 16911979 ER PT J AU Connolly, MB Hendson, G Steinbok, P AF Connolly, Mary B. Hendson, Glenda Steinbok, Paul TI Tuberous sclerosis complex: a review of the management of epilepsy with emphasis on surgical aspects SO CHILDS NERVOUS SYSTEM LA English DT Review DE epilepsy surgery; tuberous sclerosis; pathology; treatment; genetics ID POSITRON-EMISSION-TOMOGRAPHY; LONG-TERM-FOLLOW; GIANT-CELL ASTROCYTOMA; INFANTILE SPASMS; CORTICAL TUBERS; WEST-SYNDROME; HUMAN TISSUES; TSC1 GENE; HAMARTIN; CHILDREN AB Objective To review the management of epilepsy in patients with tuberous sclerosis complex (TSC) with an emphasis on surgical aspects, neuropathology, and pathogenesis. Methods Review of the literature and presentation of the authors' experience of surgery for refractory epilepsy in patients with TSC. Results TSC is a multisystem genetic disorder with variable phenotypic expression. TSC results from a mutation in the TSC1 gene on chromosome 9, which codes for hamartin, or in the TSC2 gene on chromosome 16 which codes for tuberin. The majority of the patients have TSC as a result of spontaneous genetic mutations while in one-third of the patients, the disorder is inherited in an autosomal dominant manner. Epilepsy is the most common neurological complication, and up to 80-90% of individuals with TSC develop epilepsy at some point in their lifetime. The onset of epilepsy is typically in early childhood. Infantile spasms are a very common early seizure type although partial seizures may occur. Developmental delay, intellectual impairment, autism, behavioral problems, and neuropsychiatric disorders occur commonly in individuals with TSC and may be associated with poorly controlled epilepsy. Antiepileptic drugs are the first-line management for epilepsy but the ketogenic diet, resection of one or more tubers, corpus callosotomy, and vagus nerve stimulation are other therapeutic options for individuals with poorly controlled epilepsy. C1 Univ British Columbia, Dept Pediat, Div Pediat Neurol, Vancouver, BC V5Z 1M9, Canada. British Columbia Childrens Hosp, Vancouver, BC, Canada. BC Childrens Hosp, Div Anat Pathol, Dept Pathol, Vancouver, BC V6H 2V4, Canada. BC Childrens Hosp, Dept Surg, Div Pediat Neurosurg, Vancouver, BC V6H 2V4, Canada. RP Connolly, MB (reprint author), BC Childrens Hosp, Div Neurol, 4480 Oak St, Vancouver, BC V6H 2V4, Canada. 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Genet. PD AUG PY 2006 VL 70 IS 2 BP 91 EP 97 DI 10.1111/j.1399-0004.2006.00649.x PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 061PE UT WOS:000238883900001 PM 16879188 ER PT J AU German, TP Hehman, JA AF German, Tim P. Hehman, Jessica A. TI Representational and executive selection resources in 'theory of mind': Evidence from compromised belief-desire reasoning in old age SO COGNITION LA English DT Article DE belief-desire reasoning; theory of mind; executive function; cognitive aging ID VARIANT FRONTOTEMPORAL DEMENTIA; FALSE BELIEF; STORY COMPREHENSION; INHIBITORY CONTROL; CHILDRENS THEORY; WORKING-MEMORY; YOUNG-CHILDREN; AUTISM; PERFORMANCE; COGNITION AB Effective belief-desire reasoning requires both specialized representational capacities-the capacity to represent the mental states as such-as well as executive selection processes for accurate performance on tasks requiring the prediction and explanation of the actions of social agents. Compromised belief-desire reasoning in a given population may reflect failures in either or both of these systems. We report evidence supporting this two-process model from belief-desire reasoning tasks conducted with younger and older adult populations. When task inferential complexity is held constant, neither group showed specific difficulty with reasoning about mental state content as compared with non-mental state content. However, manipulations that systematically increase executive performance demands within belief-desire reasoning caused systematic decreases in task performance in both older and younger adult groups. Moreover, the effect of increasing executive demands was disproportionately greater in the older group. Regression analysis indicated that measures of processing speed and inhibition contributed most to explaining variance in accuracy and response times in the belief-desire reasoning tasks. These results are consistent with the idea that compromised belief-desire reasoning in old age is likely the result of age-related decline in executive selection skills that supplement core mental state representational abilities, rather than as a result of failures in the representational system itself. (c) 2005 Elsevier B.V. All rights reserved. C1 Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA. RP German, TP (reprint author), Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA. 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Studies in zebrafish promise to reveal the complex network of regulatory genes and signaling pathways that direct the development of oxytocin- and vasopressin-like neurons, and provide insight into factors involved in brain disorders associated with disruption of these systems. Isotocin, which is homologous to oxytocin, is expressed early, in a simple pattern in the developing zebrafish brain. Single-minded 1 (sim1), a member of the bHLH-PAS family of transcriptional regulatory genes, is required for terminal differentiation of mammalian oxytocin cells and is a master regulator of neurogenesis in Drosophila. Here we show that sim1 is expressed in the zebrafish forebrain and is required for isotocin cell development. The expression pattern of sim1 mRNA in the embryonic forebrain is dynamic and complex, and overlaps with isotocin expression in the preoptic area. 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Dyn. PD AUG PY 2006 VL 235 IS 8 BP 2071 EP 2082 DI 10.1002/dvdy.20848 PG 12 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA 071GZ UT WOS:000239588800006 PM 16691572 ER PT J AU Doo, S Wing, YK AF Doo, Sylvia Wing, Yun Kwok TI Sleep problems of children with a pervasive developmental disorders: correlation with parental stress SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID ASPERGERS-DISORDER; AUTISM; PATTERNS; PREVALENCE; MOTHERS AB This study aimed to investigate the prevalence of sleep problems in Chinese children with pervasive developmental disorders (PDD) in Hong Kong and their relationship to parental stress. A cross-sectional survey was conducted in six child assessment centres. All parents of the children with PDD completed the Children's Sleep Habits Questionnaire, the Parenting Stress Index - Short Form, and questions on sleep practice. A total of 210 out of 250 questionnaires (response rate 84%) were returned. Mean age of the children was 3 years 6 months (SD 1y 4mo; range 2y-7y 7mo; 168 males, 25 females). The prevalence of parent-defined sleep problems in various sleep domains ranged from 9.3 to 45.6%, with 67.9% of children having significant problems in at least one sleep domain. The most common problems reported were bedtime resistance and parasomnias. Similar sleep problems occurred in all the PDD subgroups. The factor most significantly associated with sleep problems was the occurrence of sleep problems before the age of 2 years. The parents of children with PDD with sleep problems experienced a higher level of stress than those whose children had no sleep problems. A high prevalence of significant sleep problems was reported in Chinese children in Hong Kong with PDD. A higher stress level among the parents of those children with PDD with sleep problems suggests the need for systematic early detection and management of sleep problems in children with PDD. C1 Chinese Univ Hong Kong, Shatin Hosp, Dept Psychiat, Shatin, Hong Kong, Peoples R China. Chinese Univ Hong Kong, Shatin Hosp, Dept Hlth, Child Assessment Serv, Shatin, Hong Kong, Peoples R China. RP Wing, YK (reprint author), Chinese Univ Hong Kong, Shatin Hosp, Dept Psychiat, Room 7011,7th Floor, Shatin, Hong Kong, Peoples R China. 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Med. Child Neurol. PD AUG PY 2006 VL 48 IS 8 BP 650 EP 655 DI 10.1017/S001216220600137X PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 068DY UT WOS:000239353800006 PM 16836776 ER PT J AU Iafusco, D Vanelli, M Songini, M Chiari, G Cardella, F Fifi, A Lombardo, F Marinaro, A Melia, A Marsciani, A Vacca, A Prisco, F AF Iafusco, Dario Vanelli, Maurizio Songini, Marco Chiari, Giovanni Cardella, Francesca Fifi, Annarita Lombardo, Fortunato Marinaro, Annamaria Melia, Annafranca Marsciani, Alberto Vacca, Anna Prisco, Franco TI Type 1 diabetes and autism association seems to be linked to the incidence of diabetes SO DIABETES CARE LA English DT Letter C1 Univ Parma, Dept Paediat, I-43100 Parma, Italy. Univ Naples, Dept Paediat, Naples, Italy. Hosp Brotzu, Dept Internal Med, Cagliari, Italy. Italian Soc, Paediat Endocrinol & Diabetol Unit, Palermo, Italy. Italian Soc, Paediat Endocrinol & Diabetol Unit, Sassari, Italy. Italian Soc, Paediat Endocrinol & Diabetol Unit, Nuoro, Italy. Italian Soc, Paediat Endocrinol & Diabetol Unit, Rimini, Italy. Italian Soc, Paediat Endocrinol & Diabetol Unit, Cosenza, Italy. RP Vanelli, M (reprint author), Univ Parma, Dept Paediat, Viale A Gramsci,14, I-43100 Parma, Italy. 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Schissel, Holly Couch, Steve Schery, Teris TI Auditory characteristics of children with autism SO EAR AND HEARING LA English DT Article ID BRAIN-STEM RESPONSES; PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; INFANTILE-AUTISM; EVOKED-RESPONSES; DIAGNOSTIC INTERVIEW; HEARING-LOSS; PREVALENCE; DYSFUNCTION; POPULATION AB Objectives: The objectives of this study were (1) to describe the auditory characteristics of children with autism relative to those of typically developing children and (2) to describe the test-retest reliability of behavioral auditory test measures with this population of children with autism. Design: Audiometric data were obtained from 22 children diagnosed with autism and 22 of their typically developing peers. The audiologic test battery consisted of behavioral measures (i.e., visual reinforcement audiometry, tangible reinforcement operant conditioning audiometry, and conditioned play audiometry) and physiological measures (auditory brain stem response audiometry, distortion product otoacoustic emissions, and acoustic reflexes). Results: Children with autism had physiologic test results equivalent to their typically developing counterparts. That is, no differences in auditory brain stem response audiometry, distortion product otoacoustic emissions, or acoustic reflex results were noted between the children with autism and typically developing children. However, behavioral measures revealed that about half of the children diagnosed with autism presented pure-tone averages outside of normal limits (i.e., > 20 dB HL), although their response thresholds to speech were within normal limits. All behavioral test results were within normal limits (i.e., <= 20 dB HL) for the typically developing children. In addition, test-retest variability was typically 15 dB or greater for children with autism as compared with variability of 10 dB or less for most of the typically developing children. Conclusions: Children with autism demonstrated essentially equivalent results on a battery of physiological auditory tests as those obtained from typically developing children. However, on average, behavioral responses of children with autism were elevated and less reliable relative to those of typically developing children. Furthermore, approximately half of the children with autism demonstrated behavioral pure-tone averages outside of the normal hearing range (i.e., > 20 dB HL) despite having normal to near-normal hearing sensitivity as determined by other audiometric measures. C1 Vanderbilt Univ, Med Ctr, Dept Speech & Hearing Sci, Nashville, TN 37232 USA. 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PD AUG PY 2006 VL 27 IS 4 BP 430 EP 441 DI 10.1097/01.aud.0000224981.60575.d8 PG 12 WC Audiology & Speech-Language Pathology; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Otorhinolaryngology GA 062GV UT WOS:000238933500011 PM 16825892 ER PT J AU Zhao, Q Boismenu, R Rusche, JR Holmes, GL AF Zhao, Qian Boismenu, Richard Rusche, James R. Holmes, Gregory L. TI Lack of effect of secretin on kindling and seizures SO EPILEPSY & BEHAVIOR LA English DT Article DE kindling; seizures; hippocampus; epilepsy; secretin; vagus nerve ID PERVASIVE DEVELOPMENTAL DISORDER; HIPPOCAMPAL-LESIONS; ANIMAL-MODELS; RAT-BRAIN; EXPRESSION; AUTISM; AMYGDALA; EPILEPSY; SCHIZOPHRENIA; INHIBITION AB Secretin infused into rats activates neurons located in brain areas controlling autonomic function and emotion. The brain activity of secretin is mediated, at least in part, through vagal pathways. It is known that afferent stimulation of the vagus nerve results in considerable antiepileptic effects. Whether or not secretin has an effect on seizures is unknown. In this study, we evaluated the efficacy and safety of secretin as an antiepileptogenic agent in electrical kindling and as an anticonvulsant in fully kindled seizures. To assess antiepileptogenic effects, we administered secretin (10, 30, or 100 mu g/kg/dose) or normal saline intravenously 5 min before twice-daily kindling stimulation. To assess the anticonvulsant effect of secretin, we administered either normal saline or secretin (100 mu g/kg/dose) 5 min before the electrical stimulation to fully kindled rats. We observed no effect on kindling rate or afterdischarge duration. In fully kindled rats, secretin administration had no effect on kindling stage or afterdischarge duration. Thus, in the dose range used in this preliminary acute treatment study, secretin had no discernible antiepileptogenic or anticonvulsant effects. Secretin was very well tolerated in this multidose protocol. (C) 2006 Elsevier Inc. All rights reserved. C1 Dartmouth Coll Sch Med, Neurosci Ctr Dartmouth, Neurol Sect, Lebanon, NH 03756 USA. Repligen Corp, Waltham, MA USA. RP Zhao, Q (reprint author), Dartmouth Coll Sch Med, Neurosci Ctr Dartmouth, Neurol Sect, Lebanon, NH 03756 USA. 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PD AUG PY 2006 VL 9 IS 1 BP 46 EP 50 DI 10.1016/j.yebeh.2006.04.006 PG 5 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA 068MR UT WOS:000239378900006 PM 16723277 ER PT J AU Rinehart, NJ Tonge, BJ Bradshaw, JL Iansek, R Enticott, PG McGinley, J AF Rinehart, Nicole J. Tonge, Bruce J. Bradshaw, John L. Iansek, Robert Enticott, Peter G. McGinley, Jenny TI Gait function in high-functioning autism and Asperger's disorder SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE high-functioning Autism; Asperger's disorder; Gait; Parkinson's disease; cerebellum ID PARKINSONS-DISEASE; HUNTINGTONS-DISEASE; CHILDHOOD AUTISM; POSTURAL CONTROL; MOVEMENT; CHILDREN; COORDINATION; INDIVIDUALS; DISTURBANCE; DIAGNOSIS AB Gait abnormalities have been widely reported in individuals with autism and Asperger's disorder. There is controversy as to whether the cerebellum or the basal-ganglia frontostriatal regions underpin these abnormalities. This is the first direct comparison of gait and upper-body postural features in autism and Asperger's disorder. Clinical and control groups were matched according to age, height, weight, performance, and full scale IQ. Consistent with Hallet's (1993) cerebellar-gait hypothesis, the autistic group showed significantly increased stride-length variability in their gait in comparison to control and Asperger's disorder participants. No quantitative gait deficits were found for the Asperger's disorder group. In support of Damasio and Maurer's (1982) basal-ganglia frontostriatal-gait hypothesis, both clinical groups were rated as showing abnormal arm posturing, however, only the Asperger's group were rated as significantly different from controls in terms of head and trunk posturing. While DSM-IV-TR suggests that Asperger's disorder, but not autism, is associated with motoric clumsiness, our data suggest that both clinical groups are uncoordinated and lacking in motor smoothness. Gait differences in autism and Asperger's disorder were suggested to reflect differential involvement of the cerebellum, with commonalities reflecting similar involvement of the basal-ganglia frontostriatal region. C1 Monash Univ, Dept Psychol Med, Monash Med Ctr, Clayton, Vic 3168, Australia. Monash Univ, Neuropsychol Res Unit, Clayton, Vic 3168, Australia. Murdoch Childrens Res Unit, Gait Ctr Clin Res Excellence, Parkville, Vic, Australia. Monash Univ, Geriatr Res Unit, Kingston Ctr, So Hlth Monash Ageing Res Ctr, Cheltenham, Vic, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Dept Psychol Med, Monash Med Ctr, 246 Clayton Rd,Level 3,Block P, Clayton, Vic 3168, Australia. 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Child Adolesc. Psych. PD AUG PY 2006 VL 15 IS 5 BP 256 EP 264 DI 10.1007/s00787-006-0530-y PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 077GR UT WOS:000240017500002 PM 16554961 ER PT J AU Freitag, CM Kleser, C von Gontardf, A AF Freitag, Christine M. Kleser, Christina von Gontardf, Alexander TI Imitation and language abilities in adolescents with Autism Spectrum Disorder without language delay SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism spectrum disorder; imitation; language; apraxia ID DEVELOPMENTAL DISORDERS; CORTICAL ACTIVATION; ASPERGERS-SYNDROME; APRAXIA; COMMUNICATION; PERCEPTION; CHILDREN; BRAIN; FACE; INDIVIDUALS AB Introduction. Difficulties imitating gestures have been found in several studies in children and adolescents with Autism Spectrum Disorders (ASD). It has been hypothesized that imitation abilities might be precursors of language abilities in young children with autism. No study on imitation and language abilities in adolescents with ASD has been performed to date. Methods. Fifteen male adolescents with ASD, 16 male and 13 female controls were compared regarding imitation abilities of upper and lower facial movements, and language skills as assessed by the pragmatic rating scale and the Aachen Aphasia test (AAT). Results. Autism Spectrum Disorder subjects showed reduced imitation abilities of facial movements and non-meaningful combined hand-and-finger gestures. Regarding language, ASD subjects showed difficulties in AAT spontaneous speech measures and reduced pragmatic language abilities. Correlations of imitation and language measures differed between ASD, male and female controls. Conclusions. The weak and differential correlations of imitation and language measures in the three comparison groups might imply a differential organization of language and imitation networks in the three comparison groups. 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PD AUG PY 2006 VL 15 IS 5 BP 282 EP 291 DI 10.1007/s00787-006-0533-8 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 077GR UT WOS:000240017500005 PM 16554960 ER PT J AU Weiss, LA Kosova, G Delahanty, RJ Jiang, L Cook, EH Ober, C Sutcliffe, JS AF Weiss, Lauren A. Kosova, Gulum Delahanty, Ryan J. Jiang, Lan Cook, Edwin H., Jr. Ober, Carole Sutcliffe, James S. TI Variation in ITGB3 is associated with whole-blood serotonin level and autism susceptibility SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE autism; integrin beta3; serotonin; 5-HT; quantitative trait locus; platelet ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILY-BASED TESTS; PROMOTER VARIANTS; COMPLEX TRAITS; DOUBLE-BLIND; GENOME-WIDE; TRANSPORTER; LINKAGE; HYPERSEROTONEMIA; CHILDREN AB Autism is a pervasive developmental disorder affecting more males than females. Heritability estimates for autism can rise above 90%, and genes influencing the serotonin system are strong candidates for autism susceptibility genes, as drugs selectively acting on the serotonin system are some of the most effective treatments for maladaptive behaviors seen in autism. ITGB3 was recently identified as a male quantitative trait locus (QTL) for whole-blood serotonin levels in the Hutterites (P=0.0003). Here, we demonstrate associations between variation in ITGB3 and serotonin levels in two outbred samples (P=0.010 and 0.015). Lastly, we show that a coding variant of ITGB3 is associated with autism susceptibility in a large multiplex sample (P=0.00082), and that this variation has different effects in males and females (P=0.0018). C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Ctr Mol Neurosci, Nashville, TN 37232 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN USA. Vanderbilt Univ, Vanderbilt Kennedy Ctr, Nashville, TN USA. RP Sutcliffe, JS (reprint author), Vanderbilt Univ, Dept Mol Physiol & Biophys, Ctr Mol Neurosci, 702 Light Hall, Nashville, TN 37232 USA. EM james.s.sutcliffe@vanderbilt.edu RI Sutcliffe, James/C-1348-2012 OI Sutcliffe, James/0000-0001-5200-6007 CR Abney M, 2002, AM J HUM GENET, V70, P920, DOI 10.1086/339705 Abney M, 2000, AM J HUM GENET, V66, P629, DOI 10.1086/302759 Anderson GM, 2002, MOL PSYCHIATR, V7, P831, DOI 10.1038/sj.mp.4001099 Betancur C, 2002, MOL PSYCHIATR, V7, P67, DOI 10.1038/sj/mp/4000923 Cantor RM, 2005, AM J HUM GENET, V76, P1050, DOI 10.1086/430278 Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 Chavis P, 2001, NATURE, V411, P317, DOI 10.1038/35077101 Cook Edwin H. 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J. Hum. Genet. PD AUG PY 2006 VL 14 IS 8 BP 923 EP 931 DI 10.1038/sj.ejhg.5201644 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 067TU UT WOS:000239326300010 PM 16724005 ER PT J AU Buoni, S Zannolli, R de Santi, M Macucci, F Hayek, J Orsi, A Scarinci, R Buscalferri, A Cuccia, A Zappella, M Miracco, C AF Buoni, S. Zannolli, R. de Santi, M. Macucci, F. Hayek, J. Orsi, A. Scarinci, R. Buscalferri, A. Cuccia, A. Zappella, M. Miracco, C. TI Neurocutaneous syndrome with mental delay, autism, blockage in intracellular vescicular trafficking and melanosome defects SO EUROPEAN JOURNAL OF NEUROLOGY LA English DT Article DE autism; cell trafficking; intracellular vescicular compartment; melanosomes; mental delay; neurocutaneous syndrome ID ECTODERMAL DYSPLASIA SYNDROME; EPIDERMAL LANGERHANS CELLS; HERMANSKY-PUDLAK-SYNDROME; NORMAL HUMAN SKIN; TUBEROUS SCLEROSIS; BIRBECK GRANULES; LEOPARD SYNDROME; CUTIS TRICOLOR; MELANOCYTES; BIOGENESIS AB We evaluated a 11-year-old male patient with mental delay, autism and brownish and whitish skin spots. The former resembled those of neurofibromatosis, the latter those of tuberous sclerosis. The patient received a complete clinical work-up to exclude neurofibromatosis, tuberous sclerosis, or any other known neurocutaneous disease, with biochemistry, chromosome analysis and analysis of skin specimens. Being all the other tests not significant, two main ultrastructural defects were observed. The first was a blockage in intracellular vescicular trafficking with sparing of the mitochondria; the second an aberrant presence of melanosomes in vacuoles of several cell lines and abnormal transfer of these organelles to keratinocytes. This patient presented with a unique clinical picture distinct from neurofibromatosis or tuberous sclerosis or any other known neurocutaneous disease. The ultrastructural abnormalities suggested a defect in cell trafficking involving several cell lines and compartments. C1 Univ Siena, Dept Pediat, Sect Pediat Neurol, Policlin Scotte, I-53100 Siena, Italy. Azienda Osped Univ Senese, Pediat Neuropsychiat Unit, Policlin Scotte, Siena, Italy. Univ Siena, Dept Human Pathol & Oncol, Sect Pathol Anat & Istol, Policlin Scotte, I-53100 Siena, Italy. Azienda Osped Univ Senese, Policlin Scotte, Siena, Italy. Univ Siena, Dept Dermatol, I-53100 Siena, Italy. RP Zannolli, R (reprint author), Univ Siena, Dept Pediat, Sect Pediat Neurol, Policlin Scotte, I-53100 Siena, Italy. 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J. Neurol. PD AUG PY 2006 VL 13 IS 8 BP 842 EP 851 DI 10.1111/j.1468-1331.2006.01305.x PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 065VO UT WOS:000239188200015 PM 16879294 ER PT J AU Weiss, LA Ober, C Cook, EH AF Weiss, Lauren A. Ober, Carole Cook, Edwin H., Jr. TI ITGB3 shows genetic and expression interaction with SLC6A4 SO HUMAN GENETICS LA English DT Article ID WHOLE-BLOOD SEROTONIN; 1ST-DEGREE RELATIVES; AUTISTIC DISORDER; TRANSPORTER; FAMILIES; PROMOTER; PROBANDS AB Autism affects more males than females and is associated with disturbances of the serotonin system. The integrin beta 3 (ITGB3) and serotonin transporter (SLC6A4) genes were both recently identified as male quantitative trait loci (QTLs) for serotonin levels and alleles of each have been associated with autism. Here, we use publicly available genomic resources to determine whether regulation of expression level could be the mechanism behind association between serotonin level and noncoding variation in ITGB3. We also examine whether ITGB3 might interact with SLC6A4 to contribute to autism susceptibility. Using murine and human expression data, we observe that ITGB3 and SLC6A4 expression levels are correlated (0.38 < r < 0.78). Moreover, genetic variation in ITGB3 is associated with expression of both ITGB3 (P=0.012) and SLC6A4 (P=0.008) in unrelated CEPH individuals. We also show preliminary evidence that genotypes at the ITGB3 and SLC6A4 loci may interact to affect autism susceptibility (P=0.033). C1 Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. RP Weiss, LA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Human Genet Res,Psychiat & Neurodev Genet Uni, Boston, MA 02114 USA. EM laweiss@chgr.mgh.harvard.edu CR ABRAMSON RK, 1989, J AUTISM DEV DISORD, V19, P397, DOI 10.1007/BF02212938 Bradley SL, 2005, AM J MED GENET B, V136B, P58, DOI 10.1002/ajmg.b.30185 Cook Edwin H. 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Intell. Mag. PD AUG PY 2006 VL 1 IS 3 BP 41 EP 47 DI 10.1109/MCI.2006.1672987 PG 7 WC Computer Science, Artificial Intelligence SC Computer Science GA 169UC UT WOS:000246616300005 ER PT J AU Kao, HSR AF Kao, HSR TI Shufa: Chinese calligraphic handwriting (CCH) for health and behavioural therapy SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Article ID PERFORMANCE AB This paper presents an overview of psychological research on the Chinese art of calligraphy (Shufa). Using a theoretical framework, we have investigated the scientific nature of calligraphic brush handwriting as well as its treatment effects on behavioural and clinical disorders. The paper begins with an introduction to Chinese calligraphy, Chinese characters, and the character structures. This is followed by an account of a research-based framework of the psychological characteristics of Chinese calligraphy handwriting (CCH). Our basic research includes measures of the writer's physiological changes associated with the brush-writing act, and the results show that the practitioner experiences relaxation and emotional calmness evident in decelerated respiration, slower heart-rate, decreased blood pressure, and reduced muscular tension. The cognitive effects of the CCH practice included quickened response time and improved performance in discrimination and figure identification, as well as enhanced visual spatial abilities, spatial relations, abstract reasoning, and aspects of memory and attention in the practitioners. Following these findings, our applied and clinical research has resulted in positive effects of the CCH treatment on behavioural changes in individuals with autism, Attention Deficit Disorder (ADD), and Attention Deficit Hyperactivity Disorder (ADHD); on cognitive improvements in reasoning, judgement, and cognitive facilitation; and on hand steadiness in children with mild retardation; as well as enhanced memory, concentration, spatial orientation, and motor coordination in Alzheimer's patients. Similarly, we have successfully applied the CCH treatment to patients with psychosomatic diseases of hypertension and diabetes, as well as mental diseases of schizophrenia, depression, and neurosis in terms of the patients' emotions, concentration, and hospital behaviours. This new system of CCH behavioural treatment has also been applied to users of other writing systems. In summary, the present CCH research has its roots in a Chinese art, has been scientifically investigated, and offers an alternative approach to improved health. C1 Sun Yat Sen Univ, Dept Psychol, Guangzhou, Peoples R China. RP Kao, HSR (reprint author), Sun Yat Sen Univ, Dept Psychol, Guangzhou, Peoples R China. EM hrnyksr@hkucc.hku.hk CR BILLETER JF, 1990, CHINESE ART WRITING, P27 CHAU A, 1986, GRAPHONOMICS CONT RE, P273 CHEN L, 1982, SCIENCE, V218, P699, DOI 10.1126/science.7134969 Chiu ML, 2002, P 2 INT C VASC DEM S FAN ZS, 1999, CHINESE CALLIGRAPHY, P381 GAO DG, 1994, INFORM PROCESSING CH, P191 GOAN CH, 2000, INT J BEHAV MED, V7, pS1 GUO K, 1991, MOT CONTR HANDWR P 5, P30 GUO NF, 2001, ANN BEHAV MED, V23, pS2001 Guo NF, 2001, ANN BEHAV MED, V23, pS159 Kao H, 2000, INT J PSYCHOL, V35, P302 Kao H. S. 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H., 1991, DEV GRAPHIC SKILLS, P93 NR 38 TC 6 Z9 7 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD AUG PY 2006 VL 41 IS 4 BP 282 EP 286 DI 10.1080/00207590544000059 PG 5 WC Psychology, Multidisciplinary SC Psychology GA 045ST UT WOS:000237763200005 ER PT J AU McGeorge, T AF McGeorge, Tristan TI Understanding the nature of autism and Asperger's disorder: Forty years of clinical practice and pioneering research. SO INTERNATIONAL REVIEW OF PSYCHIATRY LA English DT Book Review C1 Maudsley Hosp & Inst Psychiat, London SE5 8AZ, England. RP McGeorge, T (reprint author), Maudsley Hosp & Inst Psychiat, London SE5 8AZ, England. CR RITVO E, 2006, UNDERSTANDING NATURE NR 1 TC 0 Z9 0 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 0954-0261 J9 INT REV PSYCHIATR JI Int. Rev. Psych. PD AUG PY 2006 VL 18 IS 4 BP 385 EP 385 DI 10.1080/09540260600845422 PG 1 WC Psychiatry SC Psychiatry GA 078ZG UT WOS:000240144700011 ER PT J AU Charman, T AF Charman, Tony TI Behavioral Science - Preface SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID AUTISM C1 UCL, Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. RP Charman, T (reprint author), UCL, Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BARONCOHEN S, 1996, BRIT J PSYCHIAT, V168, P158, DOI DOI 10.1192/BJP.168.2.158 NR 3 TC 0 Z9 0 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 EI 1573-3432 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2006 VL 36 IS 6 BP 711 EP 712 DI 10.1007/s10803-006-0155-5 PG 2 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300001 ER PT J AU Boger-Megiddo, I Shaw, DWW Friedman, SD Sparks, BF Artru, AA Giedd, JN Dawson, G Dager, SR AF Boger-Megiddo, Inbal Shaw, Dennis W. W. Friedman, Seth D. Sparks, Bobbi F. Artru, Alan A. Giedd, Jay N. Dawson, Geraldine Dager, Stephen R. TI Corpus callosum morphometrics in young children with autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE MRI; autism; brain structure; corpus callosum ID DIAGNOSTIC OBSERVATION SCHEDULE; SEX-DIFFERENCES; BRAIN SIZE; MRI; VOLUME; INDIVIDUALS; LIFE AB This study assessed midsagittal corpus callosum cross sectional areas in 3-4 year olds with autism spectrum disorder (ASD) compared to typically developing (TD) and developmentally delayed (DD) children. Though not different in absolute size compared to TD, ASD callosums were disproportionately small adjusted for increased ASD cerebral volume. ASD clinical subgroup analysis revealed greater proportional callosum reduction in the more severely affected autistic disorder (AD) than in pervasive developmental disorder-not otherwise specified (PDD-NOS) children. DD children had smaller absolute callosums than ASD and TD. Subregion analysis revealed widely distributed callosum differences between ASD and TD children. Results could reflect decreased inter-hemispheric connectivity or cerebral enlargement due to increase in tissues less represented in the corpus callosum in ASD. C1 Childrens Hosp & Reg Med Ctr, Dept Radiol, Seattle, WA 98105 USA. Canc Epidemiol Res Coop, Publ Hlth Sci, Seattle, WA USA. Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98195 USA. Univ Washington, Sch Med, Dept Anesthesiol, Seattle, WA 98195 USA. Univ Washington, Ctr Human Dev & Disabil, Dept Psychol, Seattle, WA 98195 USA. NIMH, Bethesda, MD 20892 USA. RP Shaw, DWW (reprint author), Childrens Hosp & Reg Med Ctr, Dept Radiol, 5C-1,4800 Sand Point Way NE, Seattle, WA 98105 USA. 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Autism Dev. Disord. PD AUG PY 2006 VL 36 IS 6 BP 733 EP 739 DI 10.1007/s10803-006-0121-2 PG 7 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300004 PM 16625438 ER PT J AU Giannotti, F Cortesi, F Cerquiglini, A Bernabei, P AF Giannotti, F. Cortesi, F. Cerquiglini, A. Bernabei, P. TI An open-label study of controlled-release melatonin in treatment of sleep disorders in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE sleep disorders; autism; melatonin treatment; long-term study ID PERVASIVE DEVELOPMENTAL DISORDERS; WAKE CYCLE DISORDERS; ELDERLY INSOMNIACS; CHILDHOOD AUTISM; RATING-SCALE; YOUNG-ADULTS; DISTURBANCES; RHYTHM; RETARDATION; ADOLESCENTS AB Long-term effectiveness of controlled-release melatonin in 25 children, aged 2.6-9.6 years with autism without other coexistent pathologies was evaluated openly. Sleep patterns were studied using Children's Sleep Habits Questionnaire (CSHQ) and sleep diaries at baseline, after 1-3-6 months melatonin treatment and 1 month after discontinuation. Sleep diary and CSHQ showed a more problematic sleep in autistic children compared with controls. During treatment sleep patterns of all children improved. After discontinuation 16 children returned to pre-treatment score, readministration of melatonin was again effective. Treatment gains were maintained at 12 and 24-month follow-ups. No adverse side effects were reported. In conclusion, controlled-release melatonin may provide an effective and well-tolerated treatment for autistic children with chronic sleep disorders. C1 Univ Roma La Sapienza, Dept Dev Neurol & Psychiat, Ctr Pediat Sleep Disorders, I-00185 Rome, Italy. Univ Roma La Sapienza, Dept Dev Neurol & Psychiat, PDD Clin, I-00185 Rome, Italy. RP Giannotti, F (reprint author), Univ Roma La Sapienza, Dept Dev Neurol & Psychiat, Ctr Pediat Sleep Disorders, Via Dabelli 108, I-00185 Rome, Italy. EM flavia.giannotti@uniroma1.it CR Akaboshi S, 2000, PSYCHIAT CLIN NEUROS, V54, P379, DOI 10.1046/j.1440-1819.2000.00723.x American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Arendt J, 1997, J BIOL RHYTHM, V12, P673, DOI 10.1177/074873049701200624 Arendt J, 2003, J NEUROENDOCRINOL, V15, P427, DOI 10.1046/j.1365-2826.2003.00987.x Cajochen C, 2003, J NEUROENDOCRINOL, V15, P432, DOI 10.1046/j.1365-2826.2003.00989.x Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 Dolberg OT, 1998, AM J PSYCHIAT, V155, P1119 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 GARFIN DG, 1988, J AUTISM DEV DISORD, V18, P367, DOI 10.1007/BF02212193 Garfinkel D, 1997, ARCH GERONTOL GERIAT, V24, P223, DOI 10.1016/S0167-4943(96)00754-6 Griffiths R, 1970, ABILITIES YOUNG CHIL HAIMOV I, 1995, SLEEP, V18, P598 Hayashi E, 2000, PSYCHIAT CLIN NEUROS, V54, P383, DOI 10.1046/j.1440-1819.2000.00725.x Hering E, 1999, J AUTISM DEV DISORD, V29, P143, DOI 10.1023/A:1023092627223 HOFFMANN A, 1999, BIOL SIGNAL RECEPT, P96 Honomichl RD, 2002, J AUTISM DEV DISORD, V32, P553, DOI 10.1023/A:1021254914276 HOSHINO Y, 1987, JPN J PSYCHIAT NEUR, V41, P237 HOSHINO Y, 1984, FOLIA PSYCHIAT NEU J, V38, P45 INUMAMA K, 1984, JAPAN J CHILD ADOLES, V25, P205 Jan JE, 1999, DEV MED CHILD NEUROL, V41, P491, DOI 10.1017/S0012162299001061 Jan JE, 2004, DEV MED CHILD NEUROL, V46, P776, DOI 10.1017/S0012162204001331 Jan JE, 2000, J PINEAL RES, V29, P34, DOI 10.1034/j.1600-079X.2000.290105.x Jan JE, 1996, J PINEAL RES, V21, P193, DOI 10.1111/j.1600-079X.1996.tb00286.x Johnson CR, 1996, CHILD ADOL PSYCH CL, V5, P673 KONSTANTAREAS MM, 1989, J CHILD PSYCHOL PSYC, V30, P459, DOI 10.1111/j.1469-7610.1989.tb00259.x LAVIE P, 1997, THERAPEUTIC POTENTIA, P149 Leiter R. 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C., 1975, ASSESSMENT INFANCY VERBELKE G, 2000, LINEAR MIXED MODELS Wiggs L, 2001, J ROY SOC MED, V94, P177 Williams PG, 2004, J SLEEP RES, V13, P265 Zhdanova IV, 1999, J PEDIATR ENDOCR MET, V12, P57 Zhdanova IV, 1997, SLEEP, V20, P899 NR 58 TC 64 Z9 65 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2006 VL 36 IS 6 BP 741 EP 752 DI 10.1007/s10803-006-0116-z PG 12 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300005 PM 16897403 ER PT J AU Grela, BG McLaughlin, KS AF Grela, Bernard G. McLaughlin, Kathryn S. TI Focused stimulation for a child with autism spectrum disorder: A treatment study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism spectrum disorder; focused stimulation; parent intervention; natural language procedures ID LANGUAGE INTERVENTION; BEHAVIOR; TODDLERS AB This study explored the use of focused stimulation as an intervention technique for a three-year-old boy diagnosed with autism spectrum disorder (ASD). His parents were trained to use focused stimulation to facilitate comprehension of what is x doing question forms. Responses to question probes were collected at both pre- and post-treatment intervals. At the beginning of the study, the child did not respond correctly to any of the target questions. Following intervention, the child made significant gains towards the target goal, but little change towards a control goal used for comparison. These findings provide preliminary support for the usefulness of focused stimulation as an intervention strategy for at least some children with ASD. C1 Univ Connecticut, Dept Commun Sci, Unit 1085, Storrs, CT 06269 USA. So Connecticut State Univ, New Haven, CT 06515 USA. RP Grela, BG (reprint author), Univ Connecticut, Dept Commun Sci, Unit 1085, 850 Bolton Rd, Storrs, CT 06269 USA. EM bgrela@uconn.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARICK JR, 2003, FOCUS AUTISM OTHER D, V8, P75 Bayley N, 1993, BAYLEY SCALES INFANT Girolametto L, 1996, J SPEECH HEAR RES, V39, P1274 Harris SL, 2002, INFANT YOUNG CHILD, V14, P11 Hepting NH, 1996, J EARLY INTERVENTION, V20, P249 KOEGEL RL, 1992, J AUTISM DEV DISORD, V22, P141, DOI 10.1007/BF01058147 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 McBride BJ, 2003, TOP EARLY CHILD SPEC, V23, P5, DOI 10.1177/027112140302300102 Pearce P S, 1996, INFANT TODDLER INTER, V6, P213 Robertson SB, 1999, J SPEECH LANG HEAR R, V42, P1234 ROGERS S, 1996, J AUTISM DEV DISABIL, V23, P243 Sparrow SS, 2000, VINELAND ADAPTIVE BE TOMASELLO M, 1987, J CHILD LANG, V14, P79 Tomasello M., 1992, 1 VERBS CASE STUDY E Wetherby Amy M., 2000, AUTISM SPECTRUM DISO, P109 Yell M., 2003, FOCUS AUTISM OTHER D, V18, P182, DOI DOI 10.1177/10883576030180030601 NR 17 TC 2 Z9 3 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2006 VL 36 IS 6 BP 753 EP 756 DI 10.1007/s10803-006-0122-1 PG 4 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300006 PM 16838131 ER PT J AU Rinehart, NJ Bellgrove, MA Tonge, BJ Brereton, AV Howells-Rankin, D Bradshaw, JL AF Rinehart, Nicole J. Bellgrove, Mark A. Tonge, Bruce J. Brereton, Avril V. Howells-Rankin, Debra Bradshaw, John L. TI An examination of movement kinematics in young people with high-functioning autism and Asperger's disorder: Further evidence for a motor planning deficit SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high-functioning autism; Asperger's disorder; movement kinematics; motor preparation kinematics; motor preparation ID CHILDHOOD AUTISM; MAGNETIC-RESONANCE; PARKINSONS-DISEASE; SHIFTING ATTENTION; SPECTRUM DISORDER; CHILDREN; BRAIN; CLUMSINESS; ADULTS; BRADYKINESIA AB This paper examines upper-body movement kinematics in individuals with high-functioning autism (HFA) and Asperger's disorder (AD). In general, the results indicate that HFA is more consistently associated with impaired motoric preparation/initiation than AD. The data further suggest that this quantitative difference in motor impairment is not necessarily underpinned by greater executive dysfunction vulnerability in autism relative to AD. Quantitative motoric dissociation between autism and AD may have down-stream effects on later stages of movement resulting in qualitative differences between these disorder groups, e.g. "motor clumsiness" in AD versus "abnormal posturing" in autism. It will be important for future research to map the developmental trajectory of motor abnormalities in these disorder groups. C1 Monash Univ, Dept Psychol Med, Ctr Dev Psychiat & Psychol, Monash Med Ctr, Clayton, Vic 3168, Australia. Trinity Coll Dublin, Dept Psychol, Dublin, Ireland. Trinity Coll Dublin, Inst Neurosci, Dublin, Ireland. Monash Univ, Dept Psychol, Neuropsychol Res Unit, Clayton, Vic 3168, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Dept Psychol Med, Ctr Dev Psychiat & Psychol, Monash Med Ctr, 246 Clayton Rd, Clayton, Vic 3168, Australia. 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Autism Dev. Disord. PD AUG PY 2006 VL 36 IS 6 BP 757 EP 767 DI 10.1007/s10803-006-0118-x PG 11 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300007 PM 16865551 ER PT J AU Lindner, JL Rosen, LA AF Lindner, Jennifer L. Rosen, Lee A. TI Decoding of emotion through facial expression, prosody and verbal content in children and adolescents with Asperger's syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger's Syndrome; decoding emotion; Perception of Emotion Test; facial expression; prosody ID SOCIAL COMPETENCE; AUTISM; RECOGNITION; PERCEPTION; EMPATHY; PEOPLE AB This study examined differences in the ability to decode emotion through facial expression, prosody, and verbal content between 14 children with Asperger's Syndrome (AS) and 16 typically developing peers. The ability to decode emotion was measured by the Perception of Emotion Test (POET), which portrayed the emotions of happy, angry, sad, and neutral among the modalities of static and dynamic facial expression, prosody, verbal content, and all modalities combined. Results revealed that children with AS had more difficulty identifying emotions through static facial expression, dynamic facial expression, and prosody than typically developing children. Results are discussed in relationship to an over-reliance on verbal content as a compensatory strategy in social interactions. Treatment implications for individuals with AS are also discussed. C1 Colorado State Univ, Ft Collins, CO 80523 USA. RP Lindner, JL (reprint author), Capstone Behav Hlth, 1941 S 42nd St,Ste 514, Omaha, NE 68105 USA. 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PD AUG PY 2006 VL 36 IS 6 BP 769 EP 777 DI 10.1007/s10803-006-0105-2 PG 9 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300008 PM 16639533 ER PT J AU Wagner, GC Reuhl, KR Cheh, M McRae, P Halladay, AK AF Wagner, George C. Reuhl, Kenneth R. Cheh, Michelle McRae, Paulette Halladay, Alycia K. TI A new neurobehavioral model of autism in mice: Pre- and postnatal exposure to sodium valproate SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE animal model; autism; sodium valproate ID SELF-INJURIOUS-BEHAVIOR; LESCH-NYHAN-SYNDROME; ANIMAL-MODELS; EARLY-LIFE; RATS; LESIONS; HIPPOCAMPAL; CEREBELLAR; CHILDREN; MEMORY AB Autism symptoms, including impairments in language development, social interactions, and motor skills, have been difficult to model in rodents. Since children exposed in utero to sodium valproate (VPA) demonstrate behavioral and neuroanatomical abnormalities similar to those seen in autism, the neurodevelopmental effects of this antiepileptic agent were examined in mice following its pre- or postnatal administration. Exposed pups were evaluated in a battery of neurodevelopmental procedures designed to assess VPA-induced retardation (wherein a behavior fails to mature on schedule), regression (wherein a behavior does mature on time but then deteriorates), or intrusions (wherein normal behaviors are overshadowed by stereotypic or self-injurious behaviors). The resulting observations were interpreted in the context of this new strategy to model autism. C1 Rutgers State Univ, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Neurosci, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Pharmacol & Toxicol, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Psychol, Piscataway, NJ 08854 USA. RP Wagner, GC (reprint author), Rutgers State Univ, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ 08854 USA. 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Autism Dev. Disord. PD AUG PY 2006 VL 36 IS 6 BP 779 EP 793 DI 10.1007/s10803-006-0117-y PG 15 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300009 PM 16609825 ER PT J AU Perkins, MR Dobbinson, S Boucher, J Bol, S Bloom, P AF Perkins, Michael R. Dobbinson, Sushie Boucher, Jill Bol, Simone Bloom, Paul TI Lexical knowledge and lexical use in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; vocabulary; artifacts; temporal concepts; conversation ID LANGUAGE IMPAIRMENT; CHILDREN; CATEGORIZATION; INTENTION AB One aspect of autistic language that has been infrequently researched is vocabulary and the conceptual knowledge underpinning individual words or word types. In this descriptive study we investigate anomalous vocabulary use in a 70,000-word corpus of conversational autistic language and examine evidence that concept formation, and hence vocabulary, is abnormal in autism. Particular attention is paid to the expression of artifact and temporal concepts which some believe may develop abnormally in autism. Little evidence is found of anomalous use of artifact terms, though errors with temporal (and also spatial) expressions are relatively common. We discuss why this may be and consider several potential explanations for why underlying lexical knowledge in autism may not necessarily be reflected in lexical use. C1 Univ Sheffield, Dept Human Commun Sci, Sheffield S10 2TN, S Yorkshire, England. Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. Manchester Metropolitan Univ, Dept Psychol & Speech Pathol, Manchester M15 6BH, Lancs, England. Yale Univ, Dept Psychol, New Haven, CT 06520 USA. RP Perkins, MR (reprint author), Univ Sheffield, Dept Human Commun Sci, Sheffield S10 2TN, S Yorkshire, England. 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Autism Dev. Disord. PD AUG PY 2006 VL 36 IS 6 BP 795 EP 805 DI 10.1007/s10803-006-0120-3 PG 11 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300010 PM 16897402 ER PT J AU Kelley, E Paul, JJ Fein, D Naigles, LR AF Kelley, Elizabeth Paul, Jennifer J. Fein, Deborah Naigles, Letitia R. TI Residual language deficits in optimal outcome children with a history of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE outcome; HFA; language; semantics; pragmatics ID YOUNG-CHILDREN; INTERVENTION PROGRAM; BEHAVIORAL TREATMENT; ASPERGERS-SYNDROME; COMMUNICATION; KNOWLEDGE; MIND; AGE; IMPAIRMENTS; ACQUISITION AB This study examined whether language deficits persist even in children with optimal outcomes. We examined a group of children with prior diagnoses on the autism spectrum who had IQs in the normal range, were in age-appropriate mainstream classes, and had improved to such an extent that they were considered to be functioning at the level of their typically developing peers. Fourteen such children between the ages of five and nine were matched on age and sex with typically developing children, and were given a battery of 10 language tests to investigate their language abilities. Results indicated that while these children's grammatical capabilities are mostly indistinguishable from their peers, they are still experiencing difficulties in pragmatic and semantic language. C1 Queens Univ, Dept Psychol, Kingston, ON K7L 3N6, Canada. Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA. RP Kelley, E (reprint author), Queens Univ, Dept Psychol, 62 Arch St,H351, Kingston, ON K7L 3N6, Canada. 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RP Anderson, GM (reprint author), Yale Child Study Ctr, 230 S Frontage Rd, New Haven, CT 06520 USA. 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Autism Dev. Disord. PD AUG PY 2006 VL 36 IS 6 BP 829 EP 830 DI 10.1007/s10803-006-0153-7 PG 2 WC Psychology, Developmental SC Psychology GA 077GY UT WOS:000240018300012 PM 16874562 ER PT J AU Whitehouse, AJO Maybery, MT Durkin, K AF Whitehouse, Andrew J. O. Maybery, Murray T. Durkin, Kevin TI Inner speech impairments in autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autistic disorder; executive function; language; inner speech ID WORKING-MEMORY; WORD-LENGTH; CHILDREN; SUPPRESSION; LANGUAGE; STIMULI; NORMS AB Background: Three experiments investigated the role of inner speech deficit in cognitive performances of children with autism. Methods: Experiment 1 compared children with autism with ability-matched controls on a verbal recall task presenting pictures and words. Experiment 2 used pictures for which the typical names were either single syllable or multisyllable. Two encoding conditions manipulated the use of verbal encoding. Experiment 3 employed a task-switching paradigm for which performance has been shown to be contingent upon inner speech. Results: In Experiment 1, children with autism demonstrated a lower picture-superiority effect compared to controls. In Experiment 2, the children with autism showed a lower word-length effect when pictures were presented alone, but a more substantial word-length effect in a condition requiring overt labelling. In Experiment 3, articulatory suppression affected the task-switching performance of the control participants only. Conclusions: Individuals with autism have limitations in their use of inner speech. C1 Univ Western Australia, Nedlands, WA 6009, Australia. Univ Strathclyde, Glasgow, Lanark, Scotland. RP Whitehouse, AJO (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. 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Psychiatry PD AUG PY 2006 VL 47 IS 8 BP 857 EP 865 DI 10.1111/j.1469-7610.2006.01624.x PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 065ID UT WOS:000239152500013 PM 16899000 ER PT J AU Anagnostou, E Esposito, K Soorya, L Chaplin, W Wasserman, S Hollander, E AF Anagnostou, Evdokia Esposito, Katherine Soorya, Latha Chaplin, William Wasserman, Stacey Hollander, Eric TI Divalproex versus placebo for the prevention of irritability associated with fluoxetine treatment in autism spectrum disorder SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter ID 5-HT3 RECEPTOR; TRIAL C1 Mt Sinai Sch Med, Seaver & NY Autism Ctr Excellence, New York, NY USA. St Johns Univ, Jamaica, NY 11439 USA. RP Anagnostou, E (reprint author), Mt Sinai Sch Med, Seaver & NY Autism Ctr Excellence, New York, NY USA. 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Clin. Psychopharmacol. PD AUG PY 2006 VL 26 IS 4 BP 444 EP 446 DI 10.1097/01.jcp.0000227703.72117.bc PG 3 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 070US UT WOS:000239551200026 PM 16855475 ER PT J AU Ortega-Tudela, JM Gomez-Ariza, CJ AF Ortega-Tudela, JM Gomez-Ariza, CJ TI Computer-assisted teaching and mathematical learning in Down Syndrome children SO JOURNAL OF COMPUTER ASSISTED LEARNING LA English DT Article DE evaluation of CAL systems; improving classroom teaching; media in education; multimedia/hypermedia systems; teaching/learning strategies ID ACADEMIC ATTAINMENTS; AUTISM; MEMORY; NUMBER AB The present study aims to explore the extent to which computer-assisted teaching facilitates the learning of basic mathematical concepts and skills in children with Down Syndrome (DS). Thus, the effectiveness of a multimedia teaching method is compared with a traditional one in the teaching of counting and cardinality abilities and concepts. In our study, two groups of DS children were trained. One of them was taught by using mathematical multimedia software whereas the other learned by means of pencil-paper-based tasks on the same material as the multimedia group. The children of both groups were evaluated before and after training sessions. The multimedia group showed a higher performance than the paper and pencil assisted teaching group on a variety of tasks and measures, suggesting a clear relation between teaching method and mathematical learning in DS children. These findings are discussed in terms of their theoretical as well as applied relevance. C1 Univ Jaen, Dept Pedag, Jaen 23071, Spain. Univ Jaen, Dept Psychol, Jaen 23071, Spain. RP Ortega-Tudela, JM (reprint author), Univ Jaen, Dept Pedag, Campus Las Lagunillas,S-N, Jaen 23071, Spain. EM jmortega@ujaen.es RI Gomez-Ariza, Carlos J./B-1621-2010 OI Gomez-Ariza, Carlos J./0000-0001-5889-7533 CR Baroody A. 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L., 1992, Journal of Computing in Childhood Education, V3 NR 47 TC 14 Z9 14 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0266-4909 J9 J COMPUT ASSIST LEAR JI J. Comput. Assist. Learn. PD AUG PY 2006 VL 22 IS 4 BP 298 EP 307 DI 10.1111/j.1365-2729.2006.00179.x PG 10 WC Education & Educational Research SC Education & Educational Research GA 059TL UT WOS:000238755000007 ER PT J AU Korb, D AF Korb, Damon TI The Autism Encyclopedia: 500+entries for parents and professionals SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review C1 Ctr Dev Minds, Los Gatos, CA USA. RP Korb, D (reprint author), Ctr Dev Minds, Los Gatos, CA USA. CR NEISWORTH JT, AUTISM ENCY 500 ENTR NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD AUG PY 2006 VL 27 IS 4 BP 357 EP 358 DI 10.1097/00004703-200608000-00014 PG 2 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 075BY UT WOS:000239858400012 ER PT J AU Sugamata, M Ihara, T Sugamata, M Takeda, K AF Sugamata, Masao Ihara, Tomomi Sugamata, Miho Takeda, Ken TI Maternal exposure to diesel exhaust leads to pathological similarity to autism in newborns SO JOURNAL OF HEALTH SCIENCE LA English DT Article DE diesel exhaust; autism; cerebellum purkinje cell; apoptosis; caspase-3 AB We have already demonstrated many diesel exhaust particles (DEPs) and some damages in brain tissues (cerebral cortex and hippocampus) of newborn mice whose mothers inhaled DE during pregnancy, and these damages have the possibilities to lead to some disorders of nervous system. In this study, we examined pathological effects on newborn brain by DE-exposure to pregnant mice, especially focused on autism. ICR pregnant mice were exposed to DE and some were exposed to clean air as a comparative control. Brain tissues (cerebellum) were obtained from the mice (housed in a clean air) born from DE-exposure and control pregnant mice, and examined with light and electron microscope. To detect apoptosis, the immunohistochemical staining for caspase-3 was performed, especially; the numbers of positive Purkinje cell in cerebellum were compared between DE-exposure and control. In DE-exposure group, numerous caspase-3 positive cells were diffusely observed and the number of positive Purkinje cells was significant large than in control. Electron microscopically, specific features of apoptosis were found in Purkinje cells in the DE-exposure group. These findings indicate that DE-exposure to pregnant mice has a severe impact on fetal brain development and, especially, numerous apoptotic Purkinje cells cause the innate deficiency of them and would involve the pathogenic backing of autism. Our results would give a grave warning that the maternal inhalation of DE is hazardous to fetuses' health and it is possible that these fetal damages carries a great risk of various disorders of nervous system afterward, such as autism. C1 Tochigi Inst Clin Pathol, Dept Pathol, Shimotsuga, Tochigi 3290112, Japan. Toho Univ, Sch Med, Dept Pathol, Omori Hosp, Tokyo 1438541, Japan. Tokyo Univ Sci, Fac Pharmaceut Sci, Dept Hyg Chem, Noda, Chiba 2788510, Japan. RP Sugamata, M (reprint author), Tochigi Inst Clin Pathol, Dept Pathol, 2308-3,Minamiakatsuka, Shimotsuga, Tochigi 3290112, Japan. EM mspathol@beige.ocn.ne.jp CR BAUMAN ML, 1991, PEDIATRICS, V87, P791 Ihara T, 1998, VIRCHOWS ARCH, V433, P443, DOI 10.1007/s004280050272 Kemper TL, 1998, J NEUROPATH EXP NEUR, V57, P645, DOI 10.1097/00005072-199807000-00001 Sugamata M, 2006, J HEALTH SCI, V52, P82, DOI 10.1248/jhs.52.82 NR 4 TC 14 Z9 14 PU PHARMACEUTICAL SOC JAPAN PI TOKYO PA 2-12-15-201 SHIBUYA, SHIBUYA-KU, TOKYO, 150, JAPAN SN 1344-9702 J9 J HEALTH SCI JI J. Health Sci. PD AUG PY 2006 VL 52 IS 4 BP 486 EP 488 DI 10.1248/jhs.52.486 PG 3 WC Toxicology SC Toxicology GA 077TN UT WOS:000240053300025 ER PT J AU Rao, A Vasudevan, DM Parvati, V Sumitra, S Dhanya, N AF Rao, A. N. Vasudevan, D. M. Parvati, V Sumitra, S. Dhanya, N. TI 2-hydroxyisobutyric acid among children born out of assisted reproductive technologies and its relation to autism SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Meeting Abstract C1 Amrita Inst Med Sci, Metab Lab, Kochi, Kerala, India. NR 0 TC 0 Z9 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PD AUG PY 2006 VL 29 SU 1 BP 60 EP 60 PG 1 WC Endocrinology & Metabolism; Genetics & Heredity SC Endocrinology & Metabolism; Genetics & Heredity GA 083OC UT WOS:000240467100213 ER PT J AU Wahlund, K Kristiansson, M AF Wahlund, Katarina Kristiansson, Marianne TI Offender characteristics in lethal violence with special reference to antisocial and autistic personality traits SO JOURNAL OF INTERPERSONAL VIOLENCE LA English DT Article DE autism spectrum disorder; antisocial personality disorder; forensic psychiatry; lethal violence ID CORTEX AB The objective of the study is to assess the relationships between personality traits, lifetime psychosocial functioning, and crime scene behavior. Thirty-five male offenders referred for forensic psychiatric assessment in Sweden (1996-2001) and assigned a main diagnosis of either antisocial personality disorder (APD) or autism spectrum disorder (AUT) were retrospectively studied. APD were subcategorized into impulsive (APDi) and controlled (APDc). Those in the AUT group were less intoxicated at the time of the crime and did not often use knives or guns compared to the APD group. Males in the APDi group were older and had a higher proportion of abuse of alcohol and drugs in biological parents, physical abuse during childhood, psychiatric contacts, and suicide attempts compared to the APDc group. In the APDi group, knives were used in the homicide compared to the use of guns in the APDc group. The results suggest differences in psychosocial functioning and crime scene characteristics related to personality traits. C1 Karolinska Inst, Dept Forens Psychiat, SE-14104 Huddinge, Sweden. RP Kristiansson, M (reprint author), Karolinska Inst, Dept Forens Psychiat, POB 4044, SE-14104 Huddinge, Sweden. EM Marianne.kristiansson@rmv.se CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Hare R. 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Violence PD AUG PY 2006 VL 21 IS 8 BP 1081 EP 1091 DI 10.1177/0886260506290289 PG 11 WC Criminology & Penology; Family Studies; Psychology, Applied SC Criminology & Penology; Family Studies; Psychology GA 067NT UT WOS:000239310600007 PM 16829668 ER PT J AU Yalof, J AF Yalof, Jed TI Case illustration of a boy with nonverbal learning disorder and Asperger's features: Neuropsychological and personality assessment SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Article ID HIGH-FUNCTIONING AUTISM; RIGHT-HEMISPHERE; DISABILITIES; CHILDREN; PROFILES; ADULTS AB I present a case study of a latency-age boy referred for assessment of a nonverbal learning disability/disorder (NLD) who also had features of Asperger's syndrome (AS). I review NLD terminology, presumed brain-behavior relationship, neuropsychological profile, and diagnosis/classification issues. I discuss the challenge of differentiating NLD from AS in relation to the client's pattern of visual-spatial, communication, social-emotional, and behavioral NLD correlates. I integrate neuropsychological and personality assessment data with interviews, observations, prior testing, and input from teacher and therapist in formulating a diagnostic impression. I discuss Rorschach (Exner, 2003) and neuropsychological consultations in relation to subtle language and interpersonal features of the client's communication style. I provide parent feedback at 18 and 24 months posttesting. I discuss implications relative to a model of school neuropsychological assessment that includes the Rorschach test. C1 Immaculata Univ, Dept Grad Psychol, Immaculata, PA 19345 USA. RP Yalof, J (reprint author), Immaculata Univ, Dept Grad Psychol, POB 682, Immaculata, PA 19345 USA. 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PD AUG PY 2006 VL 87 IS 1 BP 15 EP 34 DI 10.1207/s15327752jpa8701_02 PG 20 WC Psychology, Clinical; Psychology, Social SC Psychology GA 075JG UT WOS:000239880400002 PM 16856784 ER PT J AU Yoder, P Stone, WL AF Yoder, Paul Stone, Wendy L. TI A randomized comparison of the effect of two prelinguistic communication interventions on the acquisition of spoken communication in preschoolers, with ASD SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE autism; intervention; spoken language ID FOLLOW-UP; DEVELOPMENTAL-DISABILITIES; INTENTIONAL COMMUNICATION; CHILDREN; AUTISM; SPECTRUM; SPEECH; SYSTEM; DYADS AB Purpose: This randomized group experiment compared the efficacy of 2 communication interventions (Responsive Education and Prelinguistic Milieu Teaching [RPMT] and the Picture Exchange Communication System [PECS]) on spoken communication in 36 preschoolers with autism spectrum disorders (ASD). Method: Each treatment was delivered to children for a maximum total of 24 hr over a 6-month period. Spoken communication was assessed in a rigorous test of generalization at pretreatment, posttreatment, and 6-month follow-up periods. Results: PECS was more successful than RPMT in increasing the number of nonimitative spoken communication acts and the number of different nonimitative words used at the posttreatment period. Considering growth over all 3 measurement periods, an exploratory analysis showed that growth rate of the number of different nonimitative words was faster in the PECS group than in the RPMT group for children who began treatment with relatively high object exploration. In contrast, analogous slopes were steeper in the RPMT group than in the PECS group for children who began treatment with relatively low object exploration. C1 Vanderbilt Univ, Sch Med, Nashville, TN 37203 USA. 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PD AUG PY 2006 VL 49 IS 4 BP 698 EP 711 DI 10.1044/1092-4388(2006/051) PG 14 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 078QB UT WOS:000240117200002 PM 16908870 ER PT J AU Geier, DA Geier, MR AF Geier, DA Geier, MR TI An evaluation of the effects of thimerosal on neurodevelopmental disorders reported following DTP and Hib vaccines in comparison to DTPH vaccine in the United States SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES LA English DT Article ID DEVELOPMENTAL DISORDERS; CAUSAL ASSOCIATION; UP ANALYSIS; CELL-DEATH; AUTISM; MERCURY; PREVALENCE; POPULATION; EXPOSURE; CHILDREN AB Thimerosal is an ethylmercury (49.55% mercury by weight) preservative historically added to some vaccines. Toxicokinetic studies showed children in the United States received doses of mercury from Thimerosal-containing vaccines (TCVs) in excess of safety guidelines. In the United States during the 1990s, diphtheria-tetanus-pertussis (DTP) and Haemophilus influenzae type b (Hib) vaccines (maximally, 50 mu g mercury per joint administration) and diphtheria-tetanus-pertussis-Haemophilus influenzae type b (DTPH) vaccines (25 mu g mercury per administration) were given to children in the same childhood vaccination schedule at 2, 4, 6, and 15-18 mo, so that children receiving DTP and Hib vaccines may have maximally received an additional 100 mu g more mercury exposure from TCVs than children administered DTPH vaccines. A case-control epidemiological study of neurodevelopmental disorders (NDs) reported to the Vaccine Adverse Event Reporting System (VAERS) (online public access version; updated 31 August 2004) following administration of DTP vaccines in comparison DTPH vaccines manufactured by Lederle Laboratories (Pearl River, NY) from 1994 through 1998 was undertaken. Significantly increased odds ratios for autism, speech disorders, mental retardation, infantile spasms, and thinking abnormalities reported to VAERS were found following DTP vaccines in comparison to DTPH vaccines with minimal bias or systematic error. Additional ND research should be undertaken in the context of evaluating mercury-associated exposures, especially since in 2005 the Institute of Medicine issued a report calling into question handling of vaccine safety data by the National Immunization Program of the Centers for Disease Control and Prevention. C1 Genet Ctr Amer, Silver Spring, MD 20905 USA. MedCon Inc, Silver Spring, MD USA. George Washington Univ, Dept Biochem, Washington, DC USA. RP Geier, MR (reprint author), Genet Ctr Amer, 14 Redgate Ct, Silver Spring, MD 20905 USA. 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Toxicol. Env. Health Part A PD AUG 1 PY 2006 VL 69 IS 15 BP 1481 EP 1495 DI 10.1080/15287390500364556 PG 15 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 051XC UT WOS:000238194000005 PM 16766480 ER PT J AU Parkes, G Hall, I AF Parkes, Georgina Hall, Ian TI Gender dysphoria and cross-dressing in people with intellectual disability: A literature review SO MENTAL RETARDATION LA English DT Article ID IDENTITY DISORDER; LEARNING-DISABILITIES; MENTAL-RETARDATION; TRANSSEXUALISM; PREVALENCE; CHILDREN; NETHERLANDS; SINGAPORE; AUTISM; MALES AB In clinical practice, we have come across people with intellectual disability who have gender dysphoria and cross-dress. Here, we review the literature on this subject and present an illustrative case example. We searched databases, followed-up references from relevant articles, and contacted colleagues in the field. We found nine papers with case examples and one survey. Gender identity problems certainly occur in people with intellectual disabilities, and developmental perspectives are important in assessing and treating them. In some cases autistic spectrum disorder was comorbid, for individuals with and those without intellectual disability. Aggression was also common. Documented treatments were primarily psychological and social and did not include hormones and sex reassignment surgery. Capacity to consent is a factor that determines treatment. C1 Univ London St Georges Hosp, Sch Med, Dept Mental Hlth Learning Disabil, London SW17 0RE, England. Islington Learning Disabil, London N7 8US, England. RP Parkes, G (reprint author), Univ London St Georges Hosp, Sch Med, Dept Mental Hlth Learning Disabil, Cranmer Terrace, London SW17 0RE, England. 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Retard. PD AUG PY 2006 VL 44 IS 4 BP 260 EP 271 DI 10.1352/0047-6765(2006)44[260:GDACIP]2.0.CO;2 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 068SY UT WOS:000239395900003 PM 16834463 ER PT J AU Siebelink, EM de Jong, MDT Taal, E Roelvink, L AF Siebelink, Eline M. de Jong, Menno D. T. Taal, Erik Roelvink, Leo TI Sexuality and people with intellectual disabilities: Assessment of knowledge, attitudes, experiences, and needs SO MENTAL RETARDATION LA English DT Article ID MENTAL-RETARDATION; LEARNING-DISABILITIES; ADULTS; INDIVIDUALS; BEHAVIOR; ADOLESCENTS; CHALLENGES; FEELINGS; AUTISM; ISSUES AB The topic of sexuality and romantic relationships of people with mild to moderate intellectual disabilities was examined. We developed a questionnaire to investigate the 76 respondents' sexual knowledge, attitudes, experience, and needs. During the interviews, observational data were gathered to check the validity of the instrument. Results show that sexuality and romantic relationships are important aspects in the lives of many persons with intellectual disabilities. Male respondents generally reported more sexual needs than did females. Correlations were found between sexual knowledge and attitudes and between attitudes and experience or needs, suggesting that general behavioral models may be fruitfully used to further explore the topic of sexuality among people with intellectual disabilities. C1 Univ Twente, Fac Behav Sci, Behav Res Inst, NL-7500 AE Enschede, Netherlands. Aveleijn Fdn, NL-7622 GW Borne, Netherlands. RP Siebelink, EM (reprint author), Univ Twente, Fac Behav Sci, Behav Res Inst, POB 217, NL-7500 AE Enschede, Netherlands. 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Retard. PD AUG PY 2006 VL 44 IS 4 BP 283 EP 294 DI 10.1352/0047-6765(2006)44[283:SAPWID]2.0.CO;2 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 068SY UT WOS:000239395900005 PM 16834465 ER PT J AU Curran, S Powell, J Neale, BM Dworzynski, K Li, T Murphy, D Bolton, PF AF Curran, S. Powell, J. Neale, B. M. Dworzynski, K. Li, T. Murphy, D. Bolton, P. F. TI An association analysis of candidate genes on chromosome 15 q11-13 and autism spectrum disorder SO MOLECULAR PSYCHIATRY LA English DT Letter ID RECEPTOR SUBUNIT GENES; LINKAGE-DISEQUILIBRIUM; TRANSMISSION/DISEQUILIBRIUM TEST; GENOTYPING ERRORS; GENOMIC SCREEN; IDENTIFICATION; ABNORMALITIES; POLYMORPHISM; INDIVIDUALS; EXPRESSION C1 Inst Psychiat, SGDP, London, England. RP Curran, S (reprint author), Inst Psychiat, SGDP, London, England. 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Psychiatr. PD AUG PY 2006 VL 11 IS 8 BP 709 EP 713 DI 10.1038/sj.mp.4001839 PG 6 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 067NL UT WOS:000239309800003 PM 16868570 ER PT J AU Schmitz, B Kramer, G Helmstadter, C Jokeit, H Koch, S Luef, G Schaefer, C AF Schmitz, B. Kraemer, G. Helmstaedter, C. Jokeit, H. Koch, S. Luef, G. Schaefer, C. TI Neuropsychological outcome following intrauterine exposure to valproate SO NERVENARZT LA German DT Review DE valproate; neuropsychological developmental disturbances; intrauterine exposure; advantages vs risk; indication ID IN-UTERO; MAJOR MALFORMATIONS; ANTIEPILEPTIC DRUGS; PRENATAL EXPOSURE; CHILDREN BORN; ANIMAL-MODELS; SPINA-BIFIDA; EPILEPSY; AUTISM; PREGNANCY AB A number of recent studies suggest a link between in utero exposure to valproate (VPA) and low IQ and behavioural disorders in children of mothers with epilepsy. In this review, a commission of the German Section of the International League Against Epilepsy discusses the evidence in the literature and practical recommendations for the use of VPA in women of childbearing potential. It is concluded that despite methodological shortcomings-largely due to the complexity of the problem and small case numbers in prospective studies-the existing data are sufficiently alarming to require great caution in the use of VPA in women who could become pregnant. The underlying mechanisms of how antiepileptic drugs may lead to neurodevelopmental problems are unclear. Further prospective studies are urgently needed to clarify this clinically important issue, and a collaborative study is suggested based on the international network established by the European Registry of Antiepileptic Drugs and Pregnancy. C1 Neurol Klin & Poliklin, Charite, D-13353 Berlin, Germany. Schweizi Epilepsie Zentrum, Zurich, Switzerland. Univ Bonn, Klin Epileptol, D-5300 Bonn, Germany. Schweizer Epilepsie Zentrum, Inst Neuropsychol Diagnost & Bildgebung, Zurich, Switzerland. Vivantes Klinikum Neukolln, Diagnose & Behandlungszentrum Kinder, Berlin, Germany. Univ Klin Innsbruck, Innsbruck, Austria. Berliner Betrieb Zent Gesundheitliche Aufgabe, Pharmakovigilanz & Beratungszentrum Embryonaltoxi, Berlin, Germany. RP Schmitz, B (reprint author), Neurol Klin & Poliklin, Charite, Campus Virchow Klinikum,Augustenburger Pl 1, D-13353 Berlin, Germany. 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Geier, Mark R. TI A meta-analysis epidemiological assessment of neurodevelopmental disorders following vaccines administered from 1994 through 2000 in the United States SO NEUROENDOCRINOLOGY LETTERS LA English DT Review DE developmental delay; mercury; merthiolate; thimerosal; thiomersal ID EVENT REPORTING SYSTEM; THIMEROSAL-CONTAINING VACCINES; IN-VITRO; DEVELOPMENTAL DISORDERS; CAUSAL ASSOCIATION; CHILDHOOD VACCINES; OXIDATIVE STRESS; ADVERSE EVENTS; UP ANALYSIS; CELL-DEATH AB BACKGROUND: Thimerosal is an cthylinercury-containing compound (49.6% mercury by weight) used as at the preservative level in vaccines (0.005% to 0.01%). METHODS: Statistical modeling in a meta-analysis epidemiological assessment of the Vaccine Adverse Event Reporting System (VAERS) for neurodevelopment disorders (NDs) reported following Diplitlieria-Tetanus-whole-cell-Pertussis (DTP) vaccines in comparison to Diphtheria-Tetanus-whole-cell-Pertussis-Haemophilus Influenzae Type b (DTPH) vaccines (administered: 1994-1997) and following Thimerosal-containing Diphtheria-Tetanus-acellular-Pertussis (DTaP), vaccines in comparison to Thimerosal-free DTaP vaccines (administered: 1997-2000), was undertaken. RESULTS: Significantly increased adjusted (sex, age, vaccine type, vaccine manufacturer) risks of autism, speech disorders, mental retardation, personality disorders, thinking abnormalities, ataxia, and NDs in general, with minimal systematic error or confounding, were associated with TCV exposure. CONCLUSION: It is clear from the results of the present epidemiological study and other recently published data associating mercury exposure with childhood NDs, additional ND research should be undertaken in the context of evaluating mercury-associated exposures, especially from Thimerosal-containing vaccines. C1 Inst Chron Illnesses, Silver Spring, MD USA. RP Geier, MR (reprint author), 14 Redgate Ct, Silver Spring, MD 20905 USA. 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Lett. PD AUG PY 2006 VL 27 IS 4 BP 401 EP 413 PG 13 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 119ST UT WOS:000243034300001 PM 16807526 ER PT J AU Sliwinski, S Croonenberghs, J Christophe, A Deboutte, D Maes, M AF Sliwinski, Sonja Croonenberghs, Jan Christophe, Armand Deboutte, Dirk Maes, Michael TI Polyunsaturated fatty acids: Do they have a role in the pathophysiology of autism? SO NEUROENDOCRINOLOGY LETTERS LA English DT Article DE autism; polyunsaturated fatty acids; EPA; DHA; cytokines; serotonin ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; ALPHA-LINOLENIC ACID; AGE-RELATED-CHANGES; CEREBROSPINAL-FLUID; 5-HYDROXYINDOLEACETIC ACID; SEROTONIN TRANSPORTER; HOMOVANILLIC-ACID; MAJOR DEPRESSION; DOUBLE-BLIND; CHILDREN AB OBJECTIVES: There is now some evidence that alterations in fatty acids may play a role in the pathophysiology of autism. The aim of the present Study was to examine whether autism is accompanied by abnormalities in the composition of the polyunsaturated fatty acids (PUFAs) in plasma phospholipids. METHODS: The plasma phospholipid omega-3 ( *3) and omega-6 ( 6) PUFA fractions and the *3/*6 ratio were measured in 16 high-functioning rnale Youngsters with autism (age 12-18) and 22 healthy volunteers. Group mean differences were assessed by means of analysis of variance (ANOVA). RESULTS: In autism there was a significant increase in the fraction of C22:6*-3 (docosahexacnoic acid, DHA) and an increase in the total *3/*6 ratio. DISCUSSION: The results of this study suggest that an increase of the plasma *3 PUFAs, in particular DHA, and of the total phospholipid 6 ratio may take part in the pathophysiology of autism. One hypothesis is that an increase of *3 PUFAs may cause alterations in the serotonergic turnover and the immune response system, both known to be associated with autism. Caution must be exercised against highly concentrated omega-3 PUFAs supplementation. C1 Univ Antwerp, ZNA Middelheim, Univ Ctr Child & Adolescent Psychiat, Antwerp, Belgium. Univ Ghent, Dept Endocrinol & Nutr, B-9000 Ghent, Belgium. Univ Hosp Maastricht, Dept Psychiat, Maastricht, Netherlands. Clin Res Ctr Mental Hlth, CRC MH, Limburg, Belgium. RP Croonenberghs, J (reprint author), Univ Antwerp, Ctr Child & Adolescent Psychiat, ZNA Middelheim Lindendreef 1, B-2020 Antwerp, Belgium. EM sonja.sliwinski@hotmail.com CR Achenbach T. 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Lett. PD AUG PY 2006 VL 27 IS 4 BP 465 EP 471 PG 7 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 119ST UT WOS:000243034300009 PM 16891996 ER PT J AU Geier, DA Geier, MR AF Geier, David A. Geier, Mark R. TI A prospective assessment of porphyrins in autistic disorders: A potential marker for heavy metal exposure SO NEUROTOXICITY RESEARCH LA English DT Article DE autistic; chelation; developmental delay ID COPROPORPHYRINOGEN OXIDASE; MERCURY EXPOSURE; OXIDATIVE STRESS; THIMEROSAL; CHILDREN; POLYMORPHISMS; ASSOCIATION; METABOLISM; BIOMARKERS; TOXICITY AB Autism was recently associated with a urinary porphyrin pattern indicative of mercury toxicity in a large cohort of French children. The IRB of the Institute for Chronic Illnesses approved the present study. A total of 37 consecutive American patients (>= 7 years-old) with autism spectrum disorders (ASDs) (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-DSM IV), born from 1983-1998, that presented to the Genetic Centers of America for outpatient genetic evaluations were prospectively examined for urinary prophryin levels (LabCorp, Inc.) from June 2005-June 2006. Imaging and laboratory testing were conducted on each patient to rule-out other causal factors for their ASDs. As controls, age-, sex-, and race-matched neurotypical ASD siblings were examined. An apparent dose-response effect was observed between autism severity and increased urinary coproporphyrins. Patients with non-chelated autism (2.25-fold, 83% had levels > 2 SD above the control mean) and non-chelated ASDs (2-fold, 58% had levels > 2 SD above the control mean), but not patients with non-chelated pervasive developmental delay-not otherwise specified (PDD-NOS) or Asperger's disorder (1.4-fold, 46% had levels > 2 SD above the control mean), had significantly increased median coproporphyrin levels versus controls. A significant increase (1.7-fold) in median coproporphyrin levels was observed among non-chelated ASD patients versus chelated ASD patients. Porphyrins should be routinely clinically measured in ASDs, and potential ASD treatments should consider monitoring porphyrin levels. Additional research should be conducted to evaluate the potential role for mercury exposure in some ASDs. C1 Genet Ctr Amer, Silver Spring, MD 20905 USA. Inst Chron Illnesses, Silver Spring, MD 20905 USA. RP Geier, MR (reprint author), Genet Ctr Amer, 14 Redgate Ct, Silver Spring, MD 20905 USA. 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Res. PD AUG PY 2006 VL 10 IS 1 BP 57 EP 63 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 085SR UT WOS:000240625200006 PM 17000470 ER PT J AU Shattuck, PT AF Shattuck, P. T. TI The contribution of diagnostic substitution to the growing administrative prevalence of autism in US special education. (vol 117, pg 1028, 2006) SO PEDIATRICS LA English DT Correction CR Shattuck PT, 2006, PEDIATRICS, V117, P1028, DOI 10.1542/peds.2005-1516 NR 1 TC 1 Z9 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD AUG PY 2006 VL 118 IS 2 BP 852 EP 852 DI 10.1542/peds.2006-1720 PG 1 WC Pediatrics SC Pediatrics GA 069IW UT WOS:000239440600074 ER PT J AU Yamada, K Matsuzawa, H Uchiyama, M Kwee, IL Nakada, T AF Yamada, Kenichi Matsuzawa, Hitoshi Uchiyama, Makoto Kwee, Ingrid L. Nakada, Tsutomu TI Brain developmental abnormalities in Prader-Willi syndrome detected by diffusion tensor imaging SO PEDIATRICS LA English DT Article; Proceedings Paper CT Annual Meeting of the Society-for-Neuroscience CY NOV 12-16, 2005 CL Washington, DC SP Soc Neurosci DE Prader-Willi syndrome; brain development; diffusion tensor imaging; trace; fractional anisotropy ID ANISOTROPY; MR; MATURATION; CHILDREN; AUTISM; AXONOGRAPHY; PHYSIOLOGY; CHILDHOOD; SCLEROSIS; INTEGRITY AB OBJECTIVE. The purpose of this work was to detect brain developmental abnormalities in Prader-Willi syndrome by using diffusion tensor imaging based on a high-field MRI system. METHODS. Eight patients with Prader-Willi syndrome and 8 age- and gender-matched normal control subjects were examined using a high-field (3.0T) MRI system. Trace value and fractional anisotropy were assessed simultaneously in multiple representative brain regions: the deep gray matter (putamen, caudate head, and dorsomedial thalamus) and the white matter structures (frontal and parietal white matter, posterior limb of internal capsule, and corpus callosum). RESULTS. In Prader-Willi syndrome patients, trace value was found to be significantly higher in the left frontal white matter and the left dorsomedial thalamus, whereas fractional anisotropy was significantly reduced in the posterior limb of the internal capsule bilaterally, the right frontal white matter, and the splenium of the corpus callosum. The observed diffusivity characteristics indicate developmental abnormalities in these areas, which are highly consistent with the clinical features of Prader-Willi syndrome. CONCLUSIONS. The study provides the first objective evidence that Prader-Willi syndrome patients indeed have developmental abnormalities in specific areas of the brain, providing a new window toward understanding the pathophysiology of Prader-Willi syndrome. C1 Niigata Univ, Ctr Integrated Human Brain Sci, Brain Res Inst, Niigata 9518585, Japan. Niigata Univ, Gra Sch Med & Dent Sci, Niigata 9518585, Japan. Univ Calif Davis, Dept Neurol, Davis, CA 95616 USA. RP Nakada, T (reprint author), Niigata Univ, Ctr Integrated Human Brain Sci, Brain Res Inst, Asahimachi 1-757, Niigata 9518585, Japan. 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SO PSICOTHEMA LA Spanish DT Article ID DOUBLE ABCX MODEL; MENTAL-RETARDATION; SOCIAL SUPPORT; CHILDREN; PARENTS; DISABILITIES; PREDICTORS; HARDINESS; SENSE AB Stress in mothers of individuals with autistic spectrum disorders. The aim of this study was to analyze maternal stress in families of individuals with autism. We proposed a multi-factorial and global model based on the Double ABCX model of family stress (McCubbin & Patterson, 1983) in which, the factor aA (stressor) interacts with bB (social support) and cC (perception of stress or, in our study, sense of coherence, SOC) to produce the dependent factor xX (level of stress). Thirty-nine mothers with children diagnosed on Autistic Spectrum disorders completed four questionnaires relating to the factors. The data were statistically analyzed using path analysis. The results showed that the empirical data fitted the theoretically proposed model well. There existed a direct and positive relationship between stressor and stress. 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TI Theory of Mind (ToM) and counterfactuality deficits in schizophrenia: misperception or misinterpretation? SO PSYCHOLOGICAL MEDICINE LA English DT Article ID SOCIAL COGNITION; DYSFUNCTION; HEMISPHERE; IMPAIRMENTS; SARCASM; COMMUNICATION; RECOGNITION; PERCEPTION; GENERATION; LANGUAGE AB Background. Theory of Mind (ToM) refers to the ability to infer another person's mental state based upon interactional information. ToM deficits have been suggested to underlie crucial aspects of social interaction failure in disorders such as autism and schizophrenia, although the development of paradigms for demonstrating such deficits remains an ongoing area of research. Recent studies have explored the use of sarcasm perception, in which subjects must infer an individual's sincerity or lack thereof, as a 'real-life' index of ToM ability, and as an index of functioning of specific right hemispheric structures. Sarcastic detection ability has not previously been studied in schizophrenia, although patients have been shown to have deficits in ability to decode emotional information from speech ('affective prosody'). Method. Twenty-two schizophrenia patients and 17 control subjects were tested on their ability to detect sarcasm from spoken speech as well as measures of affective prosody and basic pitch perception. Results. Despite normal overall intelligence, patients performed substantially worse than controls in ability to detect sarcasm (d= 2(.)2), showing both decreased sensitivity (A) in detection of sincerity versus sarcasm and an increased bias (B") toward sincerity. Correlations across groups revealed significant relationships between impairments in sarcasm recognition, affective prosody and basic pitch perception. Conclusions. These findings demonstrate substantial deficits in ability to infer an internal subjective state based upon vocal modulation among subjects with schizophrenia. 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PD AUG PY 2006 VL 36 IS 8 BP 1075 EP 1083 DI 10.1017/S0033291706007653 PG 9 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 074QO UT WOS:000239827100004 PM 16700967 ER PT J AU Laviola, G Adriani, W Gaudino, C Marino, R Keller, F AF Laviola, Giovanni Adriani, Walter Gaudino, Chiara Marino, Ramona Keller, Flavio TI Paradoxical effects of prenatal acetylcholinesterase blockade on neuro-behavioral development and drug-induced stereotypies in reeler mutant mice SO PSYCHOPHARMACOLOGY LA English DT Article DE gene-environment interaction; autism; schizophrenia; chlorpyrifos-oxon; amphetamine; scopolamine ID NEONATAL CHLORPYRIFOS EXPOSURE; VENTRAL TEGMENTAL AREA; BEHAVIORAL ALTERATIONS; MUSCARINIC RECEPTORS; GESTATIONAL EXPOSURE; NUCLEUS-ACCUMBENS; D-AMPHETAMINE; MOUSE MODEL; IN-VITRO; SCHIZOPHRENIA AB Introduction Epidemiological and experimental studies support a link between genetic and epigenetic factors in vulnerability to develop enduring neurobehavioral alterations. We studied the interplay between genetic vulnerability and the prenatal exposure to a neurotoxic compound. Chlorpyrifos, a potent and reversible acetylcholinesterase blocker used as a pesticide, and the "reeler" mouse, lacking the extracellular-matrix protein Reelin, were used. Materials and methods Homozygous reeler (RL), heterozygous (HZ), and wild-type (WT) mice were prenatally exposed to chlorpytifos-oxon (CPF-O), the active metabolite of chlorpyrifos, or to vehicle (prenatal controls) on gestation days 14-16, that is, during a peak period of neurogenesis in the cerebral cortex. The offspring was reared by the natural dam and tested during infancy and at adulthood for global consequences of the prenatal exposure. Conclusion The results are consistent with complex interactions between genetic (reeler genotype) and epigenetic (prenatal exposure to CPF-O) factors. In the case of some "genetically modulated" parameters (ultrasound vocalization, amphetamine-induced locomotion, and stereotypy), exposure to CPF-O paradoxically reverted the effects produced by progressive reelin absence. Conversely, for an "epigenetically modulated" parameter (grasping reflex maturation), the effects of CPF-O exposure were counteracted by progressive reelin absence. Finally, for parameters apparently untouched by either factor alone (righting reflex latency, scopolamine-induced locomotor activity), prenatal CPF-O exposure unmasked an otherwise latent genotype dependency. This complex picture also points to reciprocal adaptations within cholinergic and dopaminergic systems during development. Data are interesting in view of recently discovered cholinergic abnormalities in autism and schizophrenia, and may suggest new avenues for early intervention. C1 Ist Super Sanita, Dept Cell Biol & Neurosci, I-00161 Rome, Italy. Univ Rome, Lab Dev Neurosci, Rome, Italy. RP Laviola, G (reprint author), Ist Super Sanita, Dept Cell Biol & Neurosci, Viale Regina Elena 299, I-00161 Rome, Italy. 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TI Sport practice in autism SO SCIENCE & SPORTS LA French DT Article; Proceedings Paper CT 1st International Scientific Conference on The Recovery Processes of Physical Activities CY AUG, 2003 CL Paris, FRANCE DE autism; sport practice ID EXECUTIVE DYSFUNCTION; BIOLOGICAL MOTION; MOTOR-SKILLS; CHILDREN; PERCEPTION; EXERCISE; DISORDER; AREAS; RECOGNITION; BEHAVIORS AB Aims. - To evaluate the interest of the sporting practice on the quality of life of the young child with autism. Current knowledge. - Autism is linked with child developmental disorders. The causes are multifactorial and among them genetical factors are important. It concerns 0.5 to 2% of the population which would represent about 30,000 to 120,000 persons in a country such as France. First described by Kanner in 1943, it shows three main symptoms: 1) disorders of communication, verbal (language) and non verbal (gestual communication, mimics); 2) disorders of socialisation: the autistic person tends to ignore other children, considered as objects; 3) resisting to changes, the child with autism is markedly disturbed by changes in his environment and tends to repeat the same activities. Associated disturbances are described such as mental retardation, sensorimotor dysfunctions, dysfunctions of the executive functions, repetitive and compulsive behaviours, epilepsy etc. The young child with autism usually lives at his parents home. The diagnosis is rarely made before 18 months. Child progresses are the best when adapted education and care is undertaken very early. Pedagogy, education and cares are performed in school environment or in institutions, but also at home and during leisure. Investigations dedicated to sport practice in autism are seldom. In this presentation, we would like answering the following questions: 1) Which problems are encountered by the autistic child during practice of physical and sport activities? 2) Which benefits does get out the child with autism from these practices? 3) Which are the best adapted practices for autistic children in sport? 4) Which policy should be developed to favour access of autistic children to sport practice. We would like to defend the idea that physical and sport practice is for persons with autism one of the most effective ways to overcome their handicaps for the following reasons: 1) it allows adapted learning in all domains where the child presents dysfunctions, such as sensorimotor, communication, socialisation; 2) it provides a deciding factor of success in the learning processes, i.e. motivation linked to the pleasure of the sport practice and to self estimation that it provides. (c) 2006 Elsevier SAS. Tous droits reserves. 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Neurosci. PD JUL 19 PY 2006 VL 26 IS 29 BP 7674 EP 7679 DI 10.1523/JNEUROSCI.1285-06.2006 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 068GE UT WOS:000239359900016 PM 16855095 ER PT J AU Sikora, DM Pettit-Kekel, K Penfield, J Merkens, LS Steiner, RD AF Sikora, Darryn M. Pettit-Kekel, Kersti Penfield, Jennifer Merkens, Louise S. Steiner, Robert D. TI The near universal presence of autism spectrum disorders in children with Smith-Lemli-Opitz syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE SLOS; autism spectrum disorders; cholesterol metabolism; sterol; neurosteroids; standardized assessments; dietary treatment ID RATING-SCALE; IDENTIFICATION; PHENOTYPE AB Smith-Lemli-Opitz syndrome (SLOS) is an autosomal recessive condition caused by a defect in cholesterol synthesis. Affected children often have malformations and mental retardation. Autistic behaviors also are evident. The purpose of the present study was to determine the prevalence of autism spectrum disorders (ASDs) in children with SLOS. Fourteen children, 3-16 years old, were evaluated using three different methods to document autistic symptoms: (a) parent interview, (b) direct observation, and Q a behavior checklist. Blood sterols were also measured at regular intervals. Each subject was determined to have Autistic Disorder, Pervasive Developmental Disorder, not otherwise specified (PDD NOS), or no diagnosis on the autism spectrum, based on DSM-IV criteria. Correlations among variables were calculated, and blood sterol levels were compared between diagnostic groups. Approximately three-fourths of the children with SLOS (71-86% depending on the evaluation method) had an ASD, about 50% diagnosed with Autistic Disorder and the rest with PDD NOS. The children's baseline cholesterol, 7-dehydrocholesterol (7-DHC), and 8-dehydrocholesterol (8-DHC) levels, and cholesterol levels following supplementation did not correlate with the presence or severity of autistic symptoms. These results suggest that most children with SLOS have some variant of autism. SLOS appears to have the most consistent relationship with autism of any single gene disorder. Therefore, a link between cholesterol metabolism and autism is suggested. With further study, these findings, together with knowledge of the genetic and biochemical defects in SLOS, will likely provide valuable insights into the causes of autism in general. (c) 2006 Wiley-Liss, Inc. C1 Oregon Hlth & Sci Univ, Dept Pediat, Portland, OR 97207 USA. Oregon Hlth & Sci Univ, Dept Mol & Med Genet, Portland, OR 97207 USA. Oregon Hlth & Sci Univ, Dept Child Dev, Portland, OR 97207 USA. Oregon Hlth & Sci Univ, Rehabil Ctr, Doernbecher Mem Hosp Children, Portland, OR USA. 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The cardinal feature of heritable ion channel disease is a periodic disturbance of rhythmic function in constitutionally hyperexcitable tissue. While the complexity of neuroanatomy obscures functional analysis of mutations causing monogenic seizure, ataxia, or migraine syndromes, extrapolation from the cardiac (Long QT [LQT]) and muscle (Periodic Paralysis) channelopathy syndromes provides a simplified predictive framework of molecular pathology electrically stabilizing potassium ion (K+) and chloride ion (Cl-) channels, likely having lesions that diminish their current, and excitatory Na+ channels, likely having gain-of-function lesions. The voltage-gated calcium channel gene family that contains CACNA1C, the newest LQT locus, causing Timothy Syndrome with a phenotype including autism, has proven to be particularly informative for its members' ability to tie the various central nervous system (CNS) phenotypes together in an interpretable fashion, now including direct extension to the classically multigenic neuropsychiatric phenotypes. Features of a promising ion channel candidate gene arise from its broad locus, gene family, nature of alleles, physiology and pharmacology, tissue expression profiled and phenotype in model organisms. KCNN3 is explored as a paradigm to consider. C1 Univ Calif Irvine, Dept Physiol, Sec Human Genet, Irvine, CA 92697 USA. Univ Calif Irvine, Dept Biophys, Sec Human Genet, Irvine, CA 92697 USA. Univ Calif Irvine, Dept Pediat, Sec Human Genet, Irvine, CA 92697 USA. RP Gargus, JJ (reprint author), Univ Calif Irvine, Dept Physiol, Sec Human Genet, 328 Sprague Bldg,839 Med Sci Court,Mail Code 4034, Irvine, CA 92697 USA. 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Psychiatry PD JUL 15 PY 2006 VL 60 IS 2 BP 177 EP 185 DI 10.1016/j.biopsych.2005.12.008 PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 064PJ UT WOS:000239101300011 PM 16497276 ER PT J AU Ramoz, N Reichert, JG Corwin, TE Smith, CJ Silverman, JM Hollander, E Buxbaum, JD AF Ramoz, Nicolas Reichert, Jennifer G. Corwin, Thomas E. Smith, Christopher J. Silverman, Jeremy M. Hollander, Eric Buxbaum, Joseph D. TI Lack of evidence for association of the serotonin transporter gene SLC6A4 with autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autistic disorder; 5-HTT; 5-HTTLPR; haplotype; obsessive-compulsive behaviors; transmission disequilibrium test ID RIGID-COMPULSIVE BEHAVIORS; WHOLE-BLOOD SEROTONIN; 1ST-DEGREE RELATIVES; REUPTAKE INHIBITORS; SUSCEPTIBILITY GENE; SPECTRUM DISORDERS; MOLECULAR-GENETICS; GENOMEWIDE SCREEN; ADOLESCENT AUTISM; LINKAGE ANALYSIS AB Background: The serotonin transporter (5-HTT) has long been considered likely to play a role in autism. hyperserotonemia has been consistently found in a proportion of autistic patients, and the use of selective serotonin reuptake inhibitors (SSRIs) can have a positive effect in treating some symptoms of autism. Specific variants of the 5-HTT gene, SLC6A4, especially the insertion-deletion 5-HTTLPR promoter locus, have been found to modulate its expression and transporter function. Methods. We examined the transmission of the short or long allele of 5-H7-TLPR locus to affected individuals, using a large cohort of 352 families. In addition, we screened five single nucleotide polymorphisms (SXPs) in the 5' region of SLC6A4 previously reported to be positively associated with autism, as well as 4 additional SNPs also in the 5' region. Results: No association of the 5-HTTLPR locus with autism was found. Furthermore, no evidence for association of any of the nine SNPs covering the SLC6A4 gene, or any (of their haplotypes, was observed in our study. Using obsessive-compulsive behaviors (OCB), severe OCBs or rigid- compulsive subsets of our cohort gave the same negative results. Conclusions. SLC6A4 variants do not appear to be significantly involved in the liability to autism. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Geriatr & Adult Dev, New York, NY 10029 USA. RP Buxbaum, JD (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, 1 Gustave L Levy Pl,Box 1668, New York, NY 10029 USA. EM Joseph.Buxbaum@mssm.edu CR ABRAMSON RK, 1989, J AUTISM DEV DISORD, V19, P397, DOI 10.1007/BF02212938 Anderson GM, 2004, INT J DEV NEUROSCI, V22, P397, DOI 10.1016/j.ijdevneu.2004.06.006 BAILEY A, 1995, PSYCHOL MED, V25, P63 Barrett JC, 2005, BIOINFORMATICS, V21, P263, DOI 10.1093/bioinformatics/bth457 Betancur C, 2002, MOL PSYCHIATR, V7, P67, DOI 10.1038/sj/mp/4000923 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Buxbaum JD, 2004, MOL PSYCHIATR, V9, P144, DOI 10.1038/sj.mp.4001465 Cantor RM, 2005, AM J HUM GENET, V76, P1050, DOI 10.1086/430278 Clayton D, 1999, AM J HUM GENET, V65, P1170, DOI 10.1086/302577 Conroy J, 2004, MOL PSYCHIATR, V9, P587, DOI 10.1038/sj.mp.4001459 Cook EH, 1997, MOL PSYCHIATR, V2, P247 Coutinho AM, 2004, MOL PSYCHIATR, V9, P264, DOI 10.1038/sj.mp.4001409 Dudbridge F, 2003, GENET EPIDEMIOL, V25, P115, DOI 10.1002/gepi.10252 Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 Gaspar P, 2003, NAT REV NEUROSCI, V4, P1002, DOI 10.1038/nrn1256 Geschwind DH, 2001, AM J HUM GENET, V69, P463, DOI 10.1086/321292 Gingrich JA, 2001, PSYCHOPHARMACOLOGY, V155, P1, DOI 10.1007/s002130000573 Hollander E, 2005, NEUROPSYCHOPHARMACOL, V30, P582, DOI 10.1038/sj.npp.1300627 Hollander E, 2003, LANCET, V362, P732, DOI 10.1016/S0140-6736(03)14236-5 Palferman S, 2001, AM J HUM GENET, V69, P570 Jones MB, 2004, AM J MED GENET B, V126B, P58, DOI 10.1002/ajmg.b.20172 Kim SJ, 2002, MOL PSYCHIATR, V7, P278, DOI 10.1038/sj/mp/4001033 Klauck SM, 1997, HUM MOL GENET, V6, P2233, DOI 10.1093/hmg/6.13.2233 Kruglyak L, 1996, AM J HUM GENET, V58, P1347 Leboyer M, 1999, BIOL PSYCHIAT, V45, P158, DOI 10.1016/S0006-3223(97)00532-5 Lesch KP, 1996, SCIENCE, V274, P1527, DOI 10.1126/science.274.5292.1527 Lord C, 2001, AM J MED GENET, V105, P36, DOI 10.1002/1096-8628(20010108)105:1<36::AID-AJMG1053>3.0.CO;2-4 Lord C, 2000, NEURON, V28, P355, DOI 10.1016/S0896-6273(00)00115-X Maestrini E, 1999, AM J MED GENET, V88, P492, DOI 10.1002/(SICI)1096-8628(19991015)88:5<492::AID-AJMG11>3.0.CO;2-X McCauley JL, 2004, AM J MED GENET B, V127B, P104, DOI 10.1002/ajmg.b.20151 Muhle R, 2004, PEDIATRICS, V113, pE472, DOI 10.1542/peds.113.5.e472 Mulder EJ, 2005, AM J MED GENET B, V133B, P93, DOI 10.1002/ajmg.b.30122 Oliphant A, 2002, BIOTECHNIQUES S, V2002, p[56, 60] Persico AM, 2002, MOL PSYCHIATR, V7, P795, DOI 10.1038/sj.mp.4001069 Purcell S, 2003, BIOINFORMATICS, V19, P149, DOI 10.1093/bioinformatics/19.1.149 RUTTER M, 1968, J CHILD PSYCHOL PSYC, V9, P1, DOI 10.1111/j.1469-7610.1968.tb02204.x Shao YJ, 2002, AM J HUM GENET, V70, P1058, DOI 10.1086/339765 Stone JL, 2004, AM J HUM GENET, V75, P1117, DOI 10.1086/426034 Sutcliffe JS, 2005, AM J HUM GENET, V77, P265, DOI 10.1086/432648 Tordjman S, 2001, MOL PSYCHIATR, V6, P434, DOI 10.1038/sj.mp.4000873 Vaswani M, 2003, PROG NEURO-PSYCHOPH, V27, P85, DOI 10.1016/S0278-5846(02)00338-X Veenstra-VanderWeele J, 2000, EUR J PHARMACOL, V410, P165, DOI 10.1016/S0014-2999(00)00814-1 Veenstra-VanderWeele J, 2004, MOL PSYCHIATR, V9, P819, DOI 10.1038/sj.mp.4001505 Weiss LA, 2004, EUR J HUM GENET, V12, P949, DOI 10.1038/sj.ejhg.5201239 Yirmiya N, 2001, AM J MED GENET, V105, P381, DOI 10.1002/ajmg.1365 Yonan AL, 2003, AM J HUM GENET, V73, P886, DOI 10.1086/378778 NR 46 TC 32 Z9 34 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD JUL 15 PY 2006 VL 60 IS 2 BP 186 EP 191 DI 10.1016/j.biopsych.2006.01.009 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 064PJ UT WOS:000239101300012 PM 16616719 ER PT J AU Delorme, R Durand, CM Betancur, C Wagner, M Ruhrmann, S Grabe, HJ Nygren, G Gillberg, C Leboyer, M Bourgeron, T Courtet, P Jollant, F Buresi, C Aubry, JM Baud, P Bondolfi, G Bertschy, G Perroud, N Malafosse, A AF Delorme, Richard Durand, Christelle M. Betancur, Catalina Wagner, Michael Ruhrmann, Stephan Grabe, Hans-Juergen Nygren, Gudrun Gillberg, Christopher Leboyer, Marion Bourgeron, Thomas Courtet, Philippe Jollant, Fabrice Buresi, Catherine Aubry, Jean-Michel Baud, Patrick Bondolfi, Guido Bertschy, Gilles Perroud, Nader Malafosse, Alain TI No human tryptophan hydroxylase-2 gene R441H mutation in a large cohort of psychiatric patients and control subjects SO BIOLOGICAL PSYCHIATRY LA English DT Article DE human tryptophan hydroxylase-2 gene; unipolar major depression; major depressive disorder; bipolar disorder; autism spectrum disorder; obsessive-compulsive disorder ID TPH2 AB Background: It was recently reported that a rare functional variant, R441H, in the human tryptophan hydroxylase-2 gene (hTPH2) could represent an important risk factor for unipolar major depression (UP) since it was originally found in 10916 of UP patients (vs. 1.4% in control subjects). Methods. We explored the occurrence of this variation in patients with affective disorders (n = 646), autism spectrum disorders (n = 224), and obsessive-compulsive disorder (OCD) (n = 201); in healthy volunteers with no psychiatric disorders (n = 246); and in an ethnic panel of control individuals from North Africa, Sub-Sabaran Africa, India, China, and Sweden (n = 2 77). Results: Surprisingly, we did not observe the R441H variant in any of the individuals screened (3188 independent chromosomes). Conclusions: Our results do not confirm the role of the R441H mutation of the bTPH2 gene in the susceptibility to UP. The absence of the variant from a large cohort of psychiatric patients and control subjects suggests that the findings reported in the original study could be due to a genotyping error or to stratification of the initial population reported. Additional data by other groups should contribute to the clarification of the discrepancy between our results and those previous published. C1 Inst Pasteur, F-75724 Paris 15, France. Univ Paris 12, INSERM, U513, Creteil, France. Univ Bonn, Dept Psychiat, D-5300 Bonn, Germany. Univ Cologne, Dept Psychiat, Cologne, Germany. Univ Greifwad, Dept Psychiat, Greifwad, Germany. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ Hosp Montpellier, Dept Psychiat, Montpellier, France. INSERM, U361, Montpellier, France. Univ Hosp Geneva, Dept Psychiat, Geneva, Switzerland. RP Delorme, R (reprint author), Inst Pasteur, 25 Rue Dr Roux, F-75724 Paris 15, France. EM delorme@im3.inserm.fr RI Wagner, Michael/E-2325-2011; Ruhrmann, Stephan/F-1461-2013 OI Ruhrmann, Stephan/0000-0002-6022-2364 CR Coon H, 2005, AM J MED GENET B, V135B, P42, DOI 10.1002/ajmg.b.30168 Patel PD, 2004, BIOL PSYCHIAT, V55, P428, DOI 10.1016/j.biopsych.2003.09.002 Walther DJ, 2003, SCIENCE, V299, P76, DOI 10.1126/science.1078197 Zhang XD, 2005, NEURON, V45, P11, DOI 10.1016/j.neuron.2004.12.014 NR 4 TC 34 Z9 36 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD JUL 15 PY 2006 VL 60 IS 2 BP 202 EP 203 DI 10.1016/j.biopsych.2005.12.014 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 064PJ UT WOS:000239101300014 PM 16581035 ER PT J AU Song, EY VanDunk, C Kuddo, T Nelson, PG AF Song, Eun Young VanDunk, Cassandra Kuddo, Thea Nelson, Phillip G. TI Measurement of CGRP in dried blood spots using a modified sandwich enzyme immunoassay SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE EIA; CGRP; dried blood spot ID GENE-RELATED PEPTIDE; MEDULLARY-THYROID CARCINOMA; HUMAN CALCITONIN; ASSAY; EXPRESSION; AUTISM AB Calcitonin gene-related peptide (CGRP) has roles as a neurotransmitter, neuromodulator and trophic factor. CGRP has been reported to be elevated in neonatal blood of children with autism or mental retardation as compared with normal subjects by recycling immuno-affinity chromatography (RIC). While CGRP detection in neonatal blood is thus important, it is not easy to detect CGRP in dried blood spots because of the limitations of sample volume and the specificity and the sensitivity of available assay systems. In the present study, we modified a "Sandwich Enzyme Immunoassay" for the purpose of detecting CGRP in blood spot eluate. We have prepared blood spots from blood collected from normal human subjects and measured CGRP level in eluates from these blood spots. Instead of a purification step, we have introduced a pre-incubation step and used washed erythrocytes as a dilution solution. The modified assay has good recovery and specificity and appropriate dilution curves. We have compared the eluate levels with levels in serum and plasma from the same individuals and find that CGRP levels in blood spot eluate were similar to those of serum and plasma. Thus, the newly modified EIA may be a useful method for the detection of CGRP in blood spot eluate. (c) 2006 Elsevier B.V. All rights reserved. C1 NICHHD, NIH, Bethesda, MD 20892 USA. NINDS, NIH, Bethesda, MD 20892 USA. Korea Res Inst Biosci & Biotechnol, Cell Biol Lab, Taejon 305600, South Korea. RP Nelson, PG (reprint author), NICHHD, NIH, Bethesda, MD 20892 USA. 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Neurosci. Methods PD JUL 15 PY 2006 VL 155 IS 1 BP 92 EP 97 DI 10.1016/j.jneumeth.2005.12.020 PG 6 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 062IT UT WOS:000238938500011 PM 16466803 ER PT J AU Kurita, H AF Kurita, Hiroshi TI Disorders of the autism spectrum SO LANCET LA English DT Editorial Material ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; TOTAL POPULATION; PREVALENCE; JAPAN; AREA C1 Zenkoku Ryoiku Sodan Ctr, Shinjuku Ku, Tokyo 1620051, Japan. RP Kurita, H (reprint author), Zenkoku Ryoiku Sodan Ctr, Shinjuku Ku, 2-2-8 Nishiwaseda, Tokyo 1620051, Japan. EM hkurita@mvf.biglobe.ne.jp CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th Baird G, 2006, LANCET, V368, P210, DOI 10.1016/S0140-6736(06)69041-7 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Gillberg C, 2006, J AUTISM DEV DISORD, V36, P429, DOI 10.1007/s10803-006-0081-6 Honda H, 2005, J CHILD PSYCHOL PSYC, V46, P572, DOI 10.1111/j.1469-7610.2005.01425.x LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Madsen KM, 2003, PEDIATRICS, V112, P604, DOI 10.1542/peds.112.3.604 MATSUISHI T, 1987, J CHILD NEUROL, V2, P268 SUGIYAMA T, 1989, J AUTISM DEV DISORD, V19, P87, DOI 10.1007/BF02212720 TANOUE Y, 1988, J AUTISM DEV DISORD, V18, P155, DOI 10.1007/BF02211943 WHO, 1993, ICD 10 CLASS MENT BE Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 14 TC 7 Z9 8 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD JUL 15 PY 2006 VL 368 IS 9531 BP 179 EP 181 DI 10.1016/S0140-6736(06)69015-6 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 064MY UT WOS:000239095000005 PM 16844468 ER PT J AU Baird, G Simonoff, E Pickles, A Chandler, S Loucas, T Meldrum, D Charman, T AF Baird, Gillian Simonoff, Emily Pickles, Andrew Chandler, Susie Loucas, Tom Meldrum, David Charman, Tony TI Prevalence of disorders of the autism spectrum in a population cohort of children in South Thames: the Special Needs and Autism Project (SNAP) SO LANCET LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PRESCHOOL-CHILDREN; EPIDEMIOLOGY AB Background Recent reports have suggested that the prevalence of autism and related spectrum disorders (ASDs) is substantially higher than previously recognised. We sought to quantify prevalence of ASDs in children in South Thames, UK. Methods Within a total population cohort of 56946 children aged 9-10 years, we screened all those with a current clinical diagnosis of ASD (n=255) or those judged to be at risk for being an undetected case (n=1515). A stratified subsample (n=255) received a comprehensive diagnostic assessment, including standardised clinical observation, and parent interview assessments of autistic symptoms, language, and intelligence quotient (IQ). Clinical consensus diagnoses of childhood autism and other ASDs were derived. We used a sample weighting procedure to estimate prevalence. Findings The prevalence of childhood autism was 38.9 per 10000 (95% CI 29.9-47.8) and that of other ASDs was 77.2 per 10000 (52.1-102.3), making the total prevalence of all AS Ds 116.1 per 10000 (90.4-141.8). A narrower definition of childhood autism, which combined clinical consensus with instrument criteria for past and current presentation, provided a prevalence of 24.8 per 10 000 (17.6-32.0). The rate of previous local identification was lowest for children of less educated parents. Interpretation Prevalence of autism and related ASDs is substantially greater than previously recognised. Whether the increase is due to better ascertainment, broadening diagnostic criteria, or increased incidence is unclear. Services in health, education, and social care will need to recognise the needs of children with some form of ASD, who constitute 1% of the child population. C1 Guys & St Thomas NHS Fdn, Newcomen Ctr, London, England. Kings Coll London, Inst Psychiat, Dept Child & Adolescent Psychiat, London WC2R 2LS, England. Univ Manchester, Div Epidemiol & Hlth Sci, Biostat Grp, Manchester, Lancs, England. Univ Reading, Sch Psychol & Clin Language Sci, Reading, Berks, England. Chatswood Assessment Ctr, Sydney, NSW, Australia. UCL, Inst Child Hlth, Behav & Brain Sci Unit, London, England. RP Baird, G (reprint author), Guys Hosp, Newcomen Ctr, London SE1 9RT, England. EM gillian.baird@gstt.nhs.uk RI Pickles, Andrew/A-9625-2011; Simonoff, Emily/B-7593-2011; Charman, Tony/A-2085-2014 OI Pickles, Andrew/0000-0003-1283-0346; Charman, Tony/0000-0003-1993-6549 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 *DEP ED SKILLS, 2005, SPEC ED NEEDS ENGL Dunn L. 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Sixteen individuals with ASD and 16 matched control participants completed a task in which pairs of face and house stimuli were present on every trial, with one of the pairs randomly assigned to attended locations and the other to unattended locations. Both mass-univariate (SPM) and region of interest analyses suggested that responses to houses were modulated by attention in both groups, but that only the control participants demonstrated attentional modulation of face-selective regions. Thus, the participants with ASD demonstrated a lack of attentional modulation which was particularly evident for the social stimulus. Analyses of effective connectivity indicated that these results were due to a failure of attention to modulate connectivity between extrastriate areas and V1. We discuss bow these results may suggest a mechanism to explain the reduced salience of social stimuli in ASD. (c) 2006 Elsevier Inc. All rights reserved. C1 UCL, Inst Cognit Neurosci, London WC1E 6BT, England. UCL, Wellcome Dept Imaging Neurosci, London WC1E 6BT, England. Univ Milan, Dept Psychol, Milan, Italy. RP Bird, G (reprint author), UCL, Inst Cognit Neurosci, London WC1E 6BT, England. EM g.bird@ucl.ac.uk RI Frith, Chris/A-2171-2009; Frith, Uta/C-1757-2008; Catmur, Caroline/J-5413-2013 OI Frith, Chris/0000-0002-8665-0690; Frith, Uta/0000-0002-9063-4466; CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey AJ, 2005, EUR J NEUROSCI, V21, P2575, DOI 10.1111/j.1460-9568.2005.04061.x Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Belmonte M. 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Urinary porphyrin levels determined by high-performance liquid chromatography were compared between diagnostic groups including internal and external control groups. Coproporphyrin levels were elevated in children with autistic disorder relative to control groups. Elevation was maintained on normalization for age or to a control herne pathway metabolite (uroporphyrin) in the same samples. The elevation was significant (P < 0.001). Porphyrin levels were unchanged in Asperger's disorder, distinguishing it from autistic disorder. The atypical molecule precoproporphyrin, aspecific indicator of heavy metal toxicity, was also elevated in autistic disorder (P < 0.001) but not significantly in Asperger's. A subgroup with autistic disorder was treated with oral dimercaptosuccinic acid (DMSA) with a view to heavy metal removal. Following DMISA there was a significant (P = 0.002) drop in urinary porphyrin excretion. These data implicate environmental toxicity in childhood autistic disorder. (c) 2006 Elsevier Inc. All rights reserved. C1 Pieta Res, Edinburgh EH10 5YW, Midlothian, Scotland. Roslin Inst, Dept Stat, Roslin EH25 9PS, Midlothian, Scotland. Assoc ARIANCE, Clichy, France. Lab Philippe Auguste, Paris, France. RP Lathe, R (reprint author), Pieta Res, POB 27069, Edinburgh EH10 5YW, Midlothian, Scotland. 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Appl. Pharmacol. PD JUL 15 PY 2006 VL 214 IS 2 BP 99 EP 108 DI 10.1016/j.taap.2006.04.008 PG 10 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 066FU UT WOS:000239215900001 PM 16782144 ER PT J AU Ruiz-Opazo, N Tonkiss, J AF Ruiz-Opazo, Nelson Tonkiss, John TI Genome-wide scan for quantitative trait loci influencing spatial navigation and social recognition memory in Dahl rats SO PHYSIOLOGICAL GENOMICS LA English DT Article DE genetics; Morris water maze; acquisition; spatial accuracy ID AUTISM SPECTRUM DISORDERS; MORRIS WATER MAZE; X-CHROMOSOME; CREB; INFORMATION; HIPPOCAMPUS; PERFORMANCE; SYNAPSES; LESIONS; SYSTEM AB The genetic determinants of learning and memory have been difficult to unravel because of the complex inheritance of these forms of cognitive behavior encompassing multiple genetic and environmental factors. Indeed, genes that can account for strain and individual variations in learning and memory are largely unknown. Here we report a genome-wide scan for quantitative trait loci ( QTLs) affecting spatial learning and memory and social recognition memory in an F-2 population derived from Dahl rats. We detected five QTLs on chromosomes 1, 8, 11, 17, and 20 affecting spatial acquisition performance and five QTLs on chromosomes 2, 3, 9, and 20 influencing spatial accuracy ( once information about the target location had been acquired). None of these QTLs overlap, indicating the existence of independent genetic determinants for these two distinct behavioral components of spatial navigation. Moreover, five QTLs affecting social recognition memory were detected, two on chromosome 9 and three on chromosome X. The chromosomal regions linked to social recognition memory performance in the rat are syntenic to regions that have been linked to autism in humans. Thus our results could have paradigmatic value in guiding the experimental investigation of similar pathways in genetic susceptibility to this disorder, which results in profound impairments in social behavior. C1 Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Dept Med,Sect Mol Med, Boston, MA 02118 USA. Boston Univ, Sch Med, Ctr Behav Dev & Mental Retardat, Boston, MA 02118 USA. RP Ruiz-Opazo, N (reprint author), Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Dept Med,Sect Mol Med, W609,700 Albany St, Boston, MA 02118 USA. 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Genomics PD JUL 12 PY 2006 VL 26 IS 2 BP 145 EP 151 DI 10.1152/physiolgenomics.00019.2006 PG 7 WC Cell Biology; Genetics & Heredity; Physiology SC Cell Biology; Genetics & Heredity; Physiology GA 063GX UT WOS:000239007600006 PM 16837653 ER PT J AU Ward, P Ayvazo, S AF Ward, Phillip Ayvazo, Shiri TI Classwide peer tutoring in physical education: Assessing its effects with kindergartners with autism SO ADAPTED PHYSICAL ACTIVITY QUARTERLY LA English DT Article ID 5TH GRADE CHILDREN; PERFORMANCE; STYLES AB Researchers, textbooks authors, and educational policy makers recommend peer tutoring as an inclusion strategy for students with autism. However, there is little, if any, research supporting these recommendations in physical education. We assessed the effects of classwide peer tutoring (CWPT) in teaching catching skills to two typically developing peers and two children diagnosed with autism in kindergarten. A single subject withdrawal design assessed the effects of CWPT on total catches and correct catches. Results show that CWPT improved total and correct catches for the two students with autism. The results for the typically developing peers were mixed. These findings, while requiring further research, provide initial evidence to support CWPT as an inclusion strategy for children with autism in physical education. C1 Ohio State Univ, Sport & Exercise Educ Dept, Columbus, OH 43210 USA. RP Ward, P (reprint author), Ohio State Univ, Sport & Exercise Educ Dept, Columbus, OH 43210 USA. EM ward.116@osu.edu RI Ward, Phillip/B-5937-2012 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bryson SE, 1998, MENT RETARD DEV D R, V4, P97, DOI 10.1002/(SICI)1098-2779(1998)4:2<97::AID-MRDD6>3.0.CO;2-U Cooper J., 1987, APPL BEHAV ANAL Crouch DW, 1997, J TEACH PHYS EDUC, V17, P26 dePaepe J. 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Phys. Act. Q. PD JUL PY 2006 VL 23 IS 3 BP 233 EP 244 PG 12 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA 066LO UT WOS:000239231300001 ER PT J AU Rode, D AF Rode, Dorena TI Are mercury amalgam fillings safe for children? An evaluation of recent research results SO ALTERNATIVE THERAPIES IN HEALTH AND MEDICINE LA English DT Article ID RANDOMIZED CLINICAL-TRIAL; DENTAL AMALGAM; EXPOSURE; POLYMORPHISM; AUTISM AB Two recent clinical trials on the safety of amalgam fillings in children found no evidence of harmful effects from mercury-containing dental fillings after following children for 5-7 years. This review suggests the studies' results are limited by (1) sample sizes that were too small to allow detection of genetic variations in mercury toxicity at a rate of 1 in 100 or lower, (2) a lack of control for other sources of mercury, and (3) a population that may have been skewed by excluding children with autism during a time when autism was escalating due, in part, to increased frequency of thimerosal-containing vaccine use. C1 EcoNugenics Inc, Res & Dev, Santa Rosa, CA USA. RP Rode, D (reprint author), EcoNugenics Inc, Res & Dev, Santa Rosa, CA USA. 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PD JUL-AUG PY 2006 VL 12 IS 4 BP 16 EP 17 PG 2 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 062EV UT WOS:000238928300002 PM 16862738 ER PT J AU Magana, S Smith, MJ AF Magana, Sandra Smith, Matthew J. TI Psychological distress and well-being of Latina and non-Latina White mothers of youth and adults with an autism spectrum disorder: Cultural attitudes towards coresidence status SO AMERICAN JOURNAL OF ORTHOPSYCHIATRY LA English DT Article DE autism; Latina; culture; caregiving and well-being ID NUTRITION EXAMINATION SURVEY; MENTAL-RETARDATION; PUERTO-RICAN; ETHNIC-DIFFERENCES; CAREGIVER STRESS; HISPANIC HEALTH; DOWN-SYNDROME; CES-D; CHILDREN; FAMILIES AB This article examined the emotional well-being of 108 Latina and non-Latina White mothers who were coresiding with a youth or adult with an autism spectrum disorder (ASD). It was hypothesized that Latina mothers would be more satisfied with coresidence than non-Latina White mothers, and that satisfaction with coresidence would mediate the relationship between ethnicity and outcomes. When controlling for demographic characteristics, non-Latina White mothers were more distressed and had lower levels of psychological well-being than Latina mothers. As hypothesized, satisfaction with coresidence mediated this difference. Qualitative analysis revealed that both groups of mothers valued family cohesion as a positive aspect of coresidence. However, Latina mothers were less likely to report negative aspects of coresidence than non-Latina White mothers. C1 Univ Wisconsin, Sch Social Work, Madison, WI 53705 USA. Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. RP Magana, S (reprint author), Univ Wisconsin, Sch Social Work, 1500 Highland Ave, Madison, WI 53705 USA. 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PD JUL PY 2006 VL 76 IS 3 BP 346 EP 357 DI 10.1037/0002-9432.76.3.346 PG 12 WC Psychiatry; Social Work SC Psychiatry; Social Work GA 112WW UT WOS:000242559600008 PM 16981813 ER PT J AU Anckarsater, H Stahlberg, O Larson, T Hakansson, C Jutblad, SB Niklasson, L Nyden, A Wentz, E Westergren, S Cloninger, CR Gillberg, C Rastam, M AF Anckarsater, H Stahlberg, O Larson, T Hakansson, C Jutblad, SB Niklasson, L Nyden, A Wentz, E Westergren, S Cloninger, CR Gillberg, C Rastam, M TI The impact of ADHD and autism spectrum disorders on temperament, character, and personality development SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID WEAK CENTRAL COHERENCE; ASPERGER-SYNDROME; 7-YEAR-OLD CHILDREN; COGNITIVE PHENOTYPE; TOTAL POPULATION; EPIDEMIOLOGY; BORDERLINE; DIAGNOSIS; SIBLINGS; DEFICITS AB Objective: The authors describe personality development and disorders in relation to symptoms of attention deficit hyperactivity disorder (ADHD) and autism spectrum disorders. Method: Consecutive adults referred for neuropsychiatric investigation (N=240) were assessed for current and lifetime ADHD and autism spectrum disorders and completed the Temperament and Character Inventory. In a subgroup of subjects (N=174), presence of axis II personality disorders was also assessed with the Structured Clinical Interview for DSM-IV Personality Disorders (SCID-II). Results: Patients with ADHD reported high novelty seeking and high harm avoidance. Patients with autism spectrum disorders reported low novelty seeking, low reward dependence, and high harm avoidance. Character scores (self-directedness and cooperativeness) were extremely low among subjects with neuropsychiatric disorders, indicating a high overall prevalence of personality disorders, which was confirmed with the SCIDII. Cluster B personality disorders were more common in subjects with ADHD, while cluster A and C disorders were more common in those with autism spectrum disorders. The overlap between DSM-IV personality disorder categories was high, and they seem less clinically useful in this context. Conclusions: ADHD and autism spectrum disorders are associated with specific temperament configurations and an increased risk of personality disorders and deficits in character maturation. C1 Malmo Univ Hosp, Forens Psychiat Clin, S-20502 Malmo, Sweden. Gothenburg Univ, Dept Child Adolescent Psychiat, S-41124 Gothenburg, Sweden. Univ Gothenburg, Inst Psychol, Gothenburg, Sweden. NSwedish Natl Healthcare & Sci, Gothenburg, Sweden. Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Yorkhill Hosp, Glasgow, Lanark, Scotland. Univ Strathclyde, Glasgow, Lanark, Scotland. RP Anckarsater, H (reprint author), Malmo Univ Hosp, Forens Psychiat Clin, Sege Pk 8A, S-20502 Malmo, Sweden. EM henrik.anckarsater@skane.se RI Anckarsater, Henrik/C-2244-2009; Cloninger, Claude/F-5357-2012 CR Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 Bazanis E, 2002, PSYCHOL MED, V32, P1395, DOI 10.1017/S0033291702006657 Briskman J, 2001, J CHILD PSYCHOL PSYC, V42, P309, DOI 10.1111/1469-7610.00724 BURGESS JW, 1992, PSYCHIAT RES, V42, P283, DOI 10.1016/0165-1781(92)90120-R Cloninger C. R., 1994, TEMPERAMENT CHARACTE CLONINGER CR, 1993, ARCH GEN PSYCHIAT, V50, P975 Cloninger CR, 2000, J PERS DISORD, V14, P99 Cloninger R. 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J. Psychiat. PD JUL PY 2006 VL 163 IS 7 BP 1239 EP 1244 DI 10.1176/appi.ajp.163.7.1239 PG 6 WC Psychiatry SC Psychiatry GA 059CX UT WOS:000238712000022 PM 16816230 ER PT J AU Haznedar, MM Buchsbaum, MS LiCalzi, EM Cartwright, C Hollander, E AF Haznedar, MM Buchsbaum, MS LiCalzi, EM Cartwright, C Hollander, E TI Volumetric analysis and three-dimensional glucose metabolic mapping of the striatum and thalamus in patients with autism spectrum disorders SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID POSITRON-EMISSION-TOMOGRAPHY; BASAL GANGLIA; BRAIN ANATOMY; MRI; CORTEX; PERFORMANCE; SCHIZOPHRENIA; CAUDATE; MEMORY; ADULTS AB Objective: In patients with autism, behavioral deficits as well as neuroimaging studies of the anterior cingulate cortex suggest ventral rather than dorsal striatal and thalamic abnormalities in structure and function. The authors used imaging studies to map volumetric and metabolic differences within the entire dorsoventral extent of the striatum and thalamus. Method: Magnetic resonance imaging (MRI) and positron emission tomography ( PET) were used to measure volumes and metabolic activity in the thalamus, caudate, and putamen in 17 patients with autism or Asperger's disorder and 17 age- and sex-matched comparison subjects. Subjects performed a serial verbal learning test during the [F-18]-fluorodeoxyglucose uptake period. The regions of interest were outlined on contiguous axial MRI slices. After PET/MRI coregistration, region-of-interest coordinates were applied to the PET scan for each individual. Between-group differences in metabolism were assessed by three-dimensional statistical probability mapping. Results: The patients with autism spectrum disorders had greater volumes of the right caudate nucleus than comparison subjects as well as a reversal of the expected left-greater-than-right hemispheric asymmetry. Patients also had lower relative glucose metabolic rates bilaterally in the ventral caudate, putamen, and thalamus. Patients with autism had lower metabolic activity in the ventral thalamus than those with Asperger's disorder, but they did not differ from comparison subjects in metabolic activity in the caudate nucleus. Conclusions: These results are consistent with a deficit in the anterior cingulate-ventral striatum-anterior thalamic pathway in patients with autism spectrum disorders. The results also suggest an important role for the caudate in helping support working-memory demands. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. RP Haznedar, MM (reprint author), Mt Sinai Sch Med, Dept Psychiat, 1 Gustav L Levy Pl,Box 1505, New York, NY 10029 USA. 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J. Psychiat. PD JUL PY 2006 VL 163 IS 7 BP 1252 EP 1263 DI 10.1176/appi.ajp.163.7.1252 PG 12 WC Psychiatry SC Psychiatry GA 059CX UT WOS:000238712000024 PM 16816232 ER PT J AU Kolevzon, A Weiser, M Gross, R Lubin, G Knobler, HY Schmeidler, J Silverman, JM Reichenberg, A AF Kolevzon, A Weiser, M Gross, R Lubin, G Knobler, HY Schmeidler, J Silverman, JM Reichenberg, A TI Effects of season of birth on autism spectrum disorders: Fact or fiction? SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID INFANTILE-AUTISM AB Objective: This study attempted to examine the relationship between month and season of birth and risk for autism spectrum disorders. Method: The cohort included all Jewish individuals born in Israel over 5 consecutive years (N=311,169) and assessed by the Israeli Draft Board as part of the mandatory assessment of eligibility for military service conducted at age 17. The outcome of autism spectrum disorders was ascertained from the Draft Board Medical Registry, which contains information about medical and psychiatric disorders for this population of adolescents. Results: There was no association between month or season of birth and the prevalence of autistic spectrum disorders. Conclusions: The findings from this historical, population-based cohort study do not support an association between season of birth and autistic spectrum disorders. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Biomath Sci, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. Chaim Sheba Med Ctr, Dept Psychiat, IL-52621 Tel Hashomer, Israel. Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY USA. Israel Def Forces, Med Corps, Tel Aviv, Israel. RP Reichenberg, A (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA. 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PD JUL PY 2006 VL 163 IS 7 BP 1288 EP U3 DI 10.1176/appi.ajp.163.7.1288 PG 3 WC Psychiatry SC Psychiatry GA 059CX UT WOS:000238712000031 PM 16816239 ER PT J AU Hardan, AY Muddasani, S Vemulapalli, M Keshavan, MS Minshew, NJ AF Hardan, AY Muddasani, S Vemulapalli, M Keshavan, MS Minshew, NJ TI An MRI study of increased cortical thickness in autism SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID BRAIN; SIZE; AGE AB Objective: The purpose of this study was to examine cortical thickness in autism in light of the postmortem evidence of cortical abnormalities of the disorder. Method: Magnetic resonance imaging (MRI) scans were acquired from 17 children with autism and 14 healthy comparison subjects, and sulcal and gyral thickness were measured for the total brain and for all lobes. Results: Increases in total cerebral sulcal and gyral thickness were observed in children with autism relative to comparison subjects. Similar findings were noted in the temporal and parietal lobes but not in the frontal and occipital lobes. Conclusions: These preliminary findings indicate that increased cortical thickness may contribute to the increased gray matter volume and total brain size that have been observed in autism and may also be related to anomalies in cortical connectivity. C1 Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. Univ Texas, Hlth Sci Ctr, Dept Psychiat, San Antonio, TX 78284 USA. Wayne State Univ, Dept Psychiat, Detroit, MI USA. Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA. RP Hardan, AY (reprint author), Stanford Univ, Dept Psychiat & Behav Sci, 401 Quarry Rd, Stanford, CA 94305 USA. EM hardanay@stanford.edu CR Aylward EH, 2002, NEUROLOGY, V59, P175 Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 Carper RA, 2002, NEUROIMAGE, V16, P1038, DOI 10.1006/nimg.2002.1099 Gervais H, 2004, NAT NEUROSCI, V7, P801, DOI 10.1038/nn1291 Hardan AY, 2004, PSYCHIAT RES-NEUROIM, V131, P263, DOI 10.1016/j.pscychresns.2004.06.001 Just MA, 2004, BRAIN, V127, P1811, DOI 10.1093/brain/awh199 Magnotta VA, 2002, COMPUT MED IMAG GRAP, V26, P251, DOI 10.1016/S0895-6111(02)00011-3 Pennington BF, 2000, J COGNITIVE NEUROSCI, V12, P223, DOI 10.1162/089892900561850 PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Rojas DC, 2002, NEUROSCI LETT, V328, P237, DOI 10.1016/S0304-3940(02)00521-9 White T, 2003, BIOL PSYCHIAT, V54, P418, DOI 10.1016/S0006-3223(03)00065-9 WIEGAND LC, 2004, BIOL PSYCHIAT, V15, P131 NR 12 TC 94 Z9 98 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JUL PY 2006 VL 163 IS 7 BP 1290 EP 1292 DI 10.1176/appi.ajp.163.7.1290 PG 3 WC Psychiatry SC Psychiatry GA 059CX UT WOS:000238712000032 PM 16816240 ER PT J AU Greenberg, JS Seltzer, MM Hong, JK Orsmond, GI AF Greenberg, Jan S. Seltzer, Marsha Mailick Hong, Jinkuk Orsmond, Gael I. TI Bidirectional effects of expressed emotion and behavior problems and symptoms in adolescents and adults with autism SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID SCHIZOPHRENIC YOUNG-ADULTS; SUBCLINICAL PSYCHOPATHOLOGY; INTELLECTUAL DISABILITIES; DIAGNOSTIC INTERVIEW; FAMILY DYNAMICS; CHILDREN; RELATIVES; DISORDERS; STABILITY; MOTHERS AB Expressed emotion measures the emotional climate of the family and is predictive of symptom levels in a range of medical and psychiatric conditions. This study extends the investigation of the effects of expressed emotion to families of individuals with autism. 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PD JUL PY 2006 VL 111 IS 4 BP 229 EP 249 DI 10.1352/0895-8017(2006)111[229:BEOEEA]2.0.CO;2 PG 21 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 064DG UT WOS:000239068800001 PM 16792426 ER PT J AU Friedman, SD Shaw, DWW Artru, AA Dawson, G Petropoulos, H Dager, SR AF Friedman, Seth D. Shaw, Dennis W. W. Artru, Alan A. Dawson, Geraldine Petropoulos, Helen Dager, Stephen R. TI Gray and white matter brain chemistry in young children with autism SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Joint Meeting of the Electroencephalography-and-Clinical-Neuroscience-Society/International-S ociety-for-NeruoImaging-in-Psychiatry CY OCT 01, 2004 CL San Diego, CA SP Electroencephalog & Clin Neurosci Soc, Int Soc NeuroImaging Psychiatry ID MAGNETIC-RESONANCE-SPECTROSCOPY; IN-VIVO; INHIBITORY ARCHITECTURE; N-ACETYLASPARTATE; SPECTRUM DISORDER; BIPOLAR DISORDER; NMR-SPECTROSCOPY; CELL MINICOLUMN; CEREBRAL-CORTEX; INDIVIDUALS AB Context: The brain pathophysiological abnormalities underlying autism remain unclear. Neuroimaging and histological studies suggest cellular abnormalities early in the course of the disease. Objective: To measure the in vivo chemical profile of gray and white matter tissues in autism. Design: Cross-sectional spectroscopic imaging study comparing 3- to 4-year-old children with autism spectrum disorder (ASD) with age-matched comparison groups of children with delayed development (DD) and typical development (TD). Setting: The University of Washington Diagnostic Imaging Sciences Center, Seattle. Participants: Forty-five 3- to 4-year-old children with ASD, 12 age-matched children with DD, and 10 age-matched children with TD. Main Outcome Measures: Estimates of gray and white matter concentrations for choline-containing compounds (Cho), creatine plus phosphocreatine, N-acetylaspartate (NAA), and myo-inositol (mI). Transverse relaxation times for Cho, creatine plus phosphocreatine, and NAA expressed relative to control subjects with TD were examined to evaluate tissue compactness. Results: The children with ASD demonstrated decreased gray matter concentrations of Cho (P <.001), creatine plus phosphocreatine (P=.02), NAA (P=.02), and mI (P=.008) compared with children with TD. Gray matter Cho transverse relaxation was also prolonged for the ASD sample compared with the TD group (P=. 01). The children with ASD demonstrated significantly decreased levels of Cho (P=. 04) and mI (P=. 008) and trend-level NAA (P=. 09) in gray matter compared with the DD group. For white matter, both children with ASD and children with DD showed a similar pattern of NAA and mI level decreases (for children with ASD vs children with TD: NAA, P=. 03; mI, P=. 04; for children with DD vs children with TD, NAA, P=. 03; mI, P=. 07). In several analyses, cerebral volume contributed significantly as a covariate. Conclusions: Reduced gray matter chemical concentrations and altered Cho transverse relaxation, in a pattern distinct from that in children with DD, suggest decreased cellularity, or density, at this early time point in ASD. Possibly reflecting shared developmental features, white matter results were common to ASD and DD groups. The relationship between cerebral volume and neurochemistry at this early time point may indicate processes related to unit scaling. C1 Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Anesthesiol, Seattle, WA 98195 USA. Univ Washington, Sch Med, Dept Psychol, Seattle, WA USA. Univ Washington, Sch Med, Dept Psychiat, Seattle, WA USA. Univ Washington, Sch Med, Dept Bioengn, Seattle, WA USA. RP Friedman, SD (reprint author), Univ Washington, Sch Med, Dept Radiol, 1100 NE 45th St NE, Seattle, WA 98105 USA. 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Gen. Psychiatry PD JUL PY 2006 VL 63 IS 7 BP 786 EP 794 DI 10.1001/archpsyc.63.7.786 PG 9 WC Psychiatry SC Psychiatry GA 059RJ UT WOS:000238749600011 PM 16818868 ER PT J AU Legoff, DB Sherman, M AF Legoff, Daniel B. Sherman, Michael TI Long-term outcome of social skills intervention based on interactive LEGO (c) play SO AUTISM LA English DT Article DE autistic spectrum disorders; LEGO (c); therapy; social skills ID BEHAVIORAL TREATMENT; CHILDREN; AUTISM; COMPETENCE; DISORDERS AB LEGO (c) building materials have been adapted as a therapeutic modality for increasing motivation to participate in social skills intervention, and providing a medium through which children with social and communication handicaps can effectively interact. A 3 year retrospective study of long-term outcome for autistic spectrum children participating in LEGO (c) therapy (N = 60) compared Vineland Adaptive Behavior Scale socialization domain (VABS-SD) and Gilliam Autism Rating Scale social interaction subscale (GARS-SI) scores pre- and post-treatment with a matched comparison sample (N = 5 7) who received comparable non-LEGO (c) therapy. Although both groups made significant gains on the two outcome measures, LEGO (c) participants improved significantly more than the comparison subjects. Diagnosis and pre-treatment full-scale IQ scores did not predict outcome scores; however, Vineland adaptive behavior composite, Vineland communication domain, and verbal IQ all predicted outcome on the VABS-SD, especially for the LEGO (c) therapy group. Results are discussed in terms of implications for methods of social skills intervention for autistic spectrum disorders. C1 Bancroft NeuroHlth, Haddonfield, NJ 08033 USA. 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G., 1999, CANADIAN J SCH PSYCH, V14, P1, DOI 10.1177/082957359901400202 NR 22 TC 15 Z9 15 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUL PY 2006 VL 10 IS 4 BP 317 EP 329 DI 10.1177/1362361306064403 PG 13 WC Psychology, Developmental SC Psychology GA 068RA UT WOS:000239390900002 PM 16908476 ER PT J AU Siaperas, P Beadle-Brown, J AF Siaperas, Panagiotis Beadle-Brown, Julie TI A case study of the use of a structured teaching approach in adults with autism in a residential home in Greece SO AUTISM LA English DT Article DE adults; autism; Greece; residential home; structured teaching; TEACCH ID CHILDREN; PROGRAM AB In November 2001, the Greek Society for the Protection of Autistic People (GSPAP) established the first residence for people with autism in Greece, following the guidelines of structured teaching and the TEACCH method with all 12 of the residents. Using interview questionnaires and systematic naturalistic observations, this case study explored the effectiveness of the training programme in the residence for the 12 adolescents and adults with autism, who had never received any other intervention or training. The instruments used for the evaluation were the Childhood Autism Rating Scale, the Vineland Adaptive Behavior Scales and structured observations. The categories evaluated were personal independence, social abilities and functional communication. After a period of 6 months the results showed significant progress in these three areas of functioning for all of the residents. The implications of the results in particular for further research and service development in Greece are discussed. C1 Univ Cambridge, Sect Dev Psychiat, Learning Disabil Res Grp, Cambridge CB2 2AH, England. Univ Kent, Canterbury CT2 7NZ, Kent, England. RP Siaperas, P (reprint author), Univ Cambridge, Sect Dev Psychiat, Learning Disabil Res Grp, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. EM panagiotis.siaperas@gmail.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BEADLEBROWN J, 2002, J INTELL DISABIL RES, V44, P12 BEASLEY F, 1993, MTS HDB OBSERVERS Davison G., 2001, ABNORMAL PSYCHOL ENGEL GL, 1980, AM J PSYCHIAT, V137, P535 FAHERTY C, 1996, VISUALLY STRUCTURED Frith U., 2003, AUTISM EXPLAINING EN Jordan R., 1999, AUTISM, V3, P101, DOI 10.1177/1362361399003001009 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Martin P, 1993, MEASURING BEHAV Mesibov G., 1988, ADOLESCENT ADULT PSY, VIV Mesibov G. 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TI Quantitative assessment of autistic symptomatology in preschoolers SO AUTISM LA English DT Article DE autism; PDD-NOS; preschool; risperidone; Social Responsiveness Scale ID PERVASIVE DEVELOPMENTAL DISORDERS; RECIPROCAL SOCIAL-BEHAVIOR; DIAGNOSTIC INTERVIEW; CHILDREN; RISPERIDONE; TRAITS; SCALE; TERM AB Given a growing emphasis on early intervention for children with autism, valid quantitative tools for measuring treatment response are needed. The Social Responsiveness Scale (SRS) is a brief (15-20 minute) quantitative measure of autistic traits in 4- to 18-year-olds, for which a version for 3-year-olds was recently developed. We obtained serial SRS measurements on 73 preschool children with (n = 51) and without (n = 22) autism spectrum conditions. Inter-rater reliability (mothers and teachers) and test-retest reliability were of the order of 0.75 (Pearson's r). There was substantial agreement between SRS scores and (1) the Vineland Adaptive Behavior Composite (Pearson's r = -0.86) and (2) scores for social impairment on the Autism Diagnostic Interview-Revised (r = 0.63). Overall, quantitative autistic trait scores tended to improve over time in preschoolers, irrespective of treatment conditions. We conclude that it is possible to obtain reliable quantitative measurements of autistic social impairment in preschoolers, suitable for assessing treatment response. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, 660 S Euclid Ave,Campus Box 8134, St Louis, MO 63110 USA. EM constantino@wustl.edu CR Constantino JN, 2004, J CHILD PSYCHOL PSYC, V45, P719, DOI 10.1111/j.1469-7610.2004.00266.x Constantino JN, 2003, J AUTISM DEV DISORD, V33, P427, DOI 10.1023/A:1025014929212 Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Constantino JN, 2000, J DEV BEHAV PEDIATR, V21, P2 Freeman BJ, 1999, J AUTISM DEV DISORD, V29, P379, DOI 10.1023/A:1023078827457 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Malone RP, 2002, J AM ACAD CHILD PSY, V41, P140, DOI 10.1097/00004583-200202000-00007 Masi G, 2003, J CLIN PSYCHIAT, V64, P1039 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Sparrow S., 1984, VINELAND SCALES ADAP Spiker D, 2002, AM J MED GENET, V114, P129, DOI 10.1002/ajmg.10188 NR 14 TC 33 Z9 33 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUL PY 2006 VL 10 IS 4 BP 344 EP 352 DI 10.1177/1362361306064434 PG 9 WC Psychology, Developmental SC Psychology GA 068RA UT WOS:000239390900004 PM 16908478 ER PT J AU Palermo, MT Pasqualetti, P Barbati, G Intelligente, F Rossini, PM AF Palermo, Mark T. Pasqualetti, Patrizio Barbati, Giulia Intelligente, Fabio Rossini, Paolo Maria TI Recognition of schematic facial displays of emotion in parents of children with autism SO AUTISM LA English DT Article DE autism; broader autism phenotype; emotion perteption; facial displays ID 1ST-DEGREE RELATIVES; PERSONALITY-CHARACTERISTICS; DEMOGRAPHIC-VARIABLES; SOCIAL-BEHAVIOR; FAMILY HISTORY; EXPRESSIONS; PERCEPTION; FACES; INDIVIDUALS; PERFORMANCE AB Performance on an emotional labeling task in response to schematic facial patterns representing five basic emotions without the concurrent presentation of a verbal category was investigated in 40 parents of children with autism and 40 matched controls. 'Autism fathers' performed worse than 'autism mothers', who performed worse than controls in decoding displays representing sadness or disgust. This indicates the need to include facial expression decoding tasks in genetic research of autism. In addition, emotional expression interactions between parents and their children with autism, particularly through play, where affect and prosody are 'physiologically' exaggerated, may stimulate development of social competence. Future studies could benefit from a combination of stimuli including photographs and schematic drawings, with and without associated verbal categories. This may allow the subdivision of patients and relatives on the basis of the amount of information needed to understand and process social-emotionally relevant information. C1 Ctr Med Parioli, I-00197 Rome, Italy. Assoc Fatebenefratelli La Ricerca, Rome, Italy. RP Palermo, MT (reprint author), Ctr Med Parioli, Via Pietro Tacchini 24, I-00197 Rome, Italy. EM marktpalermo@virgilio.it RI Pasqualetti, Patrizio/D-4496-2013; Rossini, Paolo /D-4994-2013; Barbati, Giulia/N-8418-2014 OI Rossini, Paolo /0000-0003-2665-534X; CR Adolphs R, 2001, J COGNITIVE NEUROSCI, V13, P232, DOI 10.1162/089892901564289 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asthana HS, 1998, J AFFECT DISORDERS, V48, P57, DOI 10.1016/S0165-0327(97)00140-7 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Benton A. 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Twenty adults with HTA/AS correctly answered significantly fewer theory of mind questions than 20 controls on a forced-choice response task. On a narrative task, there were no differences in the proportion of mental state words between the two groups, although the participants with HFA/AS were less inclined to provide explanations for characters' mental states. No between-group differences existed on the central coherence questions of the forced-choice response task, and the participants with HTA/AS included an equivalent proportion of explanations for non-mental state phenomena in their narratives as did controls. These results support the theory of mind deficit account of autism spectrum disorders, and suggest that difficulties in mental state attribution cannot be exclusively attributed to weak central coherence. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Beaumont, R (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. EM renae@psy.uq.edu.au CR Baron-Cohen S, 2001, INT REV RES MENT RET, V23, P169 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S, 1999, NEUROCASE, V5, P475, DOI 10.1080/13554799908402743 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Capps I, 2000, J ABNORM CHILD PSYCH, V28, P193 Capps L., 1998, AUTISM, V2, P325, DOI DOI 10.1177/1362361398024002 Craig J, 2000, ISRAEL J PSYCHIAT, V37, P64 CRAWFORD JR, 1989, BRIT J CLIN PSYCHOL, V28, P267 Crawford JR, 2001, PSYCHOL MED, V31, P451 CRAWFORD JR, 1989, PERS INDIV DIFFER, V10, P793, DOI 10.1016/0191-8869(89)90126-8 Frith U., 1983, BRIT J DEV PSYCHOL, V1, P329, DOI 10.1111/j.2044-835X.1983.tb00906.x Frith U., 1989, AUTISM EXPLAINING EN FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Happe F, 1999, PSYCHOLOGIST, V12, P540 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Happe FGE, 1997, BRIT J DEV PSYCHOL, V15, P1 HAPPE FGE, 1993, COGNITION, V48, P101, DOI 10.1016/0010-0277(93)90026-R Heavey L, 2000, J AUTISM DEV DISORD, V30, P225, DOI 10.1023/A:1005544518785 Jarrold C, 1997, J AUTISM DEV DISORD, V27, P25, DOI 10.1023/A:1025817121137 Jolliffe T, 1997, J CHILD PSYCHOL PSYC, V38, P527, DOI 10.1111/j.1469-7610.1997.tb01539.x Jolliffe T, 2001, Cogn Neuropsychiatry, V6, P193 JOLLIFFE T, 1999, VIS COGN, V8, P67 Kaland N, 2002, J CHILD PSYCHOL PSYC, V43, P517, DOI 10.1111/1469-7610.00042 Klin A, 2000, J CHILD PSYCHOL PSYC, V41, P831, DOI 10.1017/S0021963099006101 Lawson J, 2004, J AUTISM DEV DISORD, V34, P301, DOI 10.1023/B:JADD.0000029552.42724.1b Lopez B, 2003, J CHILD PSYCHOL PSYC, V44, P285, DOI 10.1111/1469-7610.00121 Losh M, 2003, J AUTISM DEV DISORD, V33, P239, DOI 10.1023/A:1024446215446 LOVELAND KA, 1990, BRIT J DEV PSYCHOL, V8, P9 MINSHEW NJ, 1995, NEUROPSYCHOLOGY, V9, P255, DOI 10.1037//0894-4105.9.2.255 Mottron L, 1999, J CHILD PSYCHOL PSYC, V40, P203, DOI 10.1017/S0021963098003333 Mottron L, 2000, J CHILD PSYCHOL PSYC, V41, P1057, DOI 10.1017/S0021963099006253 Murray H. 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Mundy, Peter C. Van Hecke, Amy Vaughan Durcicher, Jennifer Stella TI Social attribution processes and comorbid psychiatric symptoms in children with Asperger syndrome SO AUTISM LA English DT Article DE Asperger syndrome; comorbid symptoms; social information processing ID HIGH-FUNCTIONING CHILDREN; SCHIZOID PERSONALITY; SPECTRUM DISORDERS; CONDUCT DISORDER; AGGRESSIVE BOYS; AUTISM; MIND; ADOLESCENTS; MECHANISMS; CHILDHOOD AB The factors that place children with Asperger syndrome at risk for comorbid psychiatric symptoms, such as anxiety and depression, remain poorly understood. We investigated the possibility that the children's emotional and behavioral difficulties are associated with social information and attribution processing. Participants were children with either Asperger syndrome (n = 31) or typical development (n = 33). To assess social information and attribution processing, children responded to hypothetical social vignettes. They also completed self-report measures of social difficulties and psychological functioning. Their parents provided information on social competence and clinical presentation. Children with Asperger syndrome showed poor psychosocial adjustment, which was related to their social information and attribution processing patterns. Cognitive and social-cognitive abilities were associated with aspects of social information processing tendencies, but not with emotional and behavioral difficulties. Results suggest that the comorbid symptoms of children with Asperger syndrome may be associated with their social perception, understanding, and experience. C1 Tavistock Clin, London NW3 5BA, England. UCL, Inst Child Hlth, Dev Psychopathol Res Unit, London NW3 5BA, England. Univ Miami, Coral Gables, FL 33124 USA. RP Meyer, JA (reprint author), Tavistock Clin, 120 Belsize Lane, London NW3 5BA, England. 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T., 2000, ASPERGER SYNDROME, P172 Shure MB, 1992, I CAN PROBLEM SOLVE Sigman M, 1999, MONOGRAPHS SOC RES C, V64, pv, DOI 10.1111/1540-5834.00001 SPICER D, 1998, ASPERGER SYNDROME HI, P377 SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 Tantam D., 2000, AUTISM INT J RES PRA, V4, P47, DOI DOI 10.1177/1362361300004001004 Tantam D, 2003, CHILD ADOL PSYCH CL, V12, P143, DOI 10.1016/S1056-4993(02)00053-6 TONGE B, 1999, AUTISM, V3, P17 TURKAT ID, 1990, J PSYCHOPATHOL BEHAV, V12, P263, DOI 10.1007/BF00960623 Klin A, 2003, CHILD ADOL PSYCH CL, V12, P1, DOI 10.1016/S1056-4993(02)00052-4 Volkmar FR, 2000, AM J PSYCHIAT, V157, P262, DOI 10.1176/appi.ajp.157.2.262 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WING L, 1981, PSYCHOL MED, V11, P115 WOLFF S, 1980, PSYCHOL MED, V10, P85 WOLFF S, 1995, J CHILD PSYCHOL PSYC, V36, P793, DOI 10.1111/j.1469-7610.1995.tb01330.x NR 75 TC 52 Z9 53 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUL PY 2006 VL 10 IS 4 BP 383 EP 402 DI 10.1177/1362361306064435 PG 20 WC Psychology, Developmental SC Psychology GA 068RA UT WOS:000239390900007 PM 16908481 ER PT J AU Jennes-Coussens, M Magill-Evans, J Koning, C AF Jennes-Coussens, Marieke Magill-Evans, Joyce Koning, Cyndie TI The quality of life of young men with Asperger syndrome - A brief report SO AUTISM LA English DT Article DE Asperger syndrome; quality of life; social support; young adults ID WHOQOL-BREF; AUTISM; POPULATION; CHILDREN; ADULTS AB Factors influencing quality of life for persons with Asperger syndrome are not yet understood. Men, ages 18 to 21, completed the World Health Organization Quality Of Life measure, the Perceived Support Network Inventory, and a semi-structured interview, Asperger syndrome affects quality of life beyond the obvious social impact. The 12 men with Asperger syndrome reported a significantly lower social and physical quality of life than did the 13 men in the control group. Education, living arrangements, and number of friends were remarkably similar between groups. Those with Asperger syndrome had less positive employment experiences and showed more preference for solitary activities. Interventions need to be based on a holistic model. C1 Univ Alberta, Fac Rehabil Med, Edmonton, AB T6G 2G4, Canada. Artevelde Hogesch Gent, Ghent, Belgium. Glenrose Rehabil Hosp, Edmonton, AB, Canada. RP Magill-Evans, J (reprint author), Univ Alberta, Fac Rehabil Med, Room 2-64 Corbett Hall, Edmonton, AB T6G 2G4, Canada. EM joyce.magill-evans@ualberta.ca CR ALISANSKI S, 2000, FOCUS AUTISM OTHER D, V15, P9 American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BERNARD J, 2001, IGNORED INELIGIBLE R Bryson S. E., 2000, AUTISM, V4, P117, DOI DOI 10.1177/1362361300004002002 CAUSE AM, 1994, SOCIAL NETWORKS CHIL, P89 CICHETTI DV, 1995, J CHILD PSYCHOL PSYC, V36, P1127 COLLINS D, 2000, TRANSITION ADULTHOOD, P3 DALRYMPLE NJ, 1996, FOCUS AUTISM OTHER D, V11, P3 Dunn W, 2002, AM J OCCUP THER, V56, P97 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Engstrom I, 2003, AUTISM, V7, P99, DOI 10.1177/1362361303007001008 Fombonne E, 2001, J AUTISM DEV DISORD, V31, P363 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P651, DOI 10.1007/BF01046333 GOODE S, 1998, AUTISM PERVASIVE DEV, P209 Grandin T., 1995, TEACHING CHILDREN AU, P33 Green D, 2002, J CHILD PSYCHOL PSYC, V43, P655, DOI 10.1111/1469-7610.00054 Hollingshead A. B., 1975, 4 FACTOR INDEX SOCIA Howlin P, 2003, J AUTISM DEV DISORD, V33, P3, DOI 10.1023/A:1022270118899 Howlin P, 2000, AUTISM, V4, P63, DOI DOI 10.1177/1362361300004001005 Howlin P, 2004, J CHILD PSYCHOL PSYC, V45, P212, DOI 10.1111/j.1469-7610.2004.00215.x Kilian R, 2001, CLIN PSYCHOL PSYCHOT, V8, P206, DOI 10.1002/cpp.277 Koning C, 2001, OCCUP THER J RES, V21, P49 Mawhood L, 1999, AUTISM INT J RES PRA, V3, P229, DOI DOI 10.1177/1362361399003003003 MCCOLL MW, 1997, OCCUPATIONAL THERAPY, P412 *MELB WHOQ FIELD S, 2002, WHO QUAL LIFE WHOQOL Myles B. S., 2002, FOCUS AUTISM OTHER D, V17, P132, DOI 10.1177/10883576020170030201 Myles BS, 2001, EDUC TRAIN MENT RET, V36, P304 Nordin V, 1998, ACTA PSYCHIAT SCAND, V97, P99, DOI 10.1111/j.1600-0447.1998.tb09970.x Nowlin P, 2005, AUTISM ASPERGER SYND O'Carroll RE, 2000, QUAL LIFE RES, V9, P121, DOI 10.1023/A:1008901320492 ORRITT EJ, 1985, AM J COMMUN PSYCHOL, V13, P565 *STAT CAN, 2001, LAB EMPL UN *STAT CAN, 1995, PORTR PERS DIS Stoddart K, 1999, AUTISM, V3, P255, DOI DOI 10.1177/1362361399003003004 SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 Tantam D., 2000, AUTISM INT J RES PRA, V4, P47, DOI DOI 10.1177/1362361300004001004 Tantam D., 1991, AUTISM ASPERGER SYND, P147, DOI 10.1017/CBO9780511526770.005 Harper A, 1998, PSYCHOL MED, V28, P551 Wechsler D., 1991, WESCHLER INTELLIGENC NR 40 TC 42 Z9 42 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUL PY 2006 VL 10 IS 4 BP 403 EP 414 DI 10.1177/1362361306064432 PG 12 WC Psychology, Developmental SC Psychology GA 068RA UT WOS:000239390900008 PM 16908482 ER PT J AU Williams, J Allison, C Scott, F Stott, C Bolton, P Baron-Cohen, S Brayne, C AF Williams, Jo Allison, Carrie Scott, Fiona Stott, Carol Bolton, Patrick Baron-Cohen, Simon Brayne, Carol TI The Childhood Asperger Syndrome Test (CAST) - Test-retest reliability SO AUTISM LA English DT Article DE Asperger syndrome; autism; childhood screening; pervasive developmental disorder; reliability ID AUTISM SPECTRUM DISORDERS; SCHOOL-AGE-CHILDREN; FUNCTIONING AUTISM; QUESTIONNAIRE; AGREEMENT AB The Childhood Asperger Syndrome Test (CAST) is a 37-item parental self-completion questionnaire to screen for autism spectrum conditions in research. Good test accuracy was demonstrated in studies with primary school aged children in mainstream schools. The aim of this study was to investigate the test-retest reliability of the CAST. Parents of 1000 children in years 1-6 in five mainstream primary schools in Cambridgeshire received the CAST. A second identical questionnaire was posted to respondents after approximately 2 weeks. Both mailings generated 136 responses. Agreement above and below a screening cut-point of 15 was investigated. The kappa statistic for agreement (< 15 versus >= 15) was 0.70, and 97 percent (95 percent CI: 93-99 percent) of children did not move across the cut-point of 15. The correlation between the two test scores was 0.83 (Spearman's rho). The CAST has shown good test-retest reliability, and now requires further investigation in a high-scoring sample. C1 Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB2 2SR, England. RP Williams, J (reprint author), Univ Cambridge, Dept Publ Hlth & Primary Care, Forvie Site,Robinson Way, Cambridge CB2 2SR, England. EM j.g.williams.97@cantab.net RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 CR Altman D, 1991, PRACTICAL STAT MED R Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 COHEN J, 1968, PSYCHOL BULL, V70, P213, DOI 10.1037/h0026256 Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 Luteijn E, 2000, J AUTISM DEV DISORD, V30, P317, DOI 10.1023/A:1005527300247 BLAND JM, 1986, LANCET, V1, P307 *NAT SCREEN COMM C, 2003, NAT SCREEN COMM POL NORMAN GR, 2000, BIOST BAR ESS Nylander L, 2001, ACTA PSYCHIAT SCAND, V103, P428, DOI 10.1034/j.1600-0447.2001.00175.x Scott FJ, 2002, AUTISM, V6, P9, DOI 10.1177/1362361302006001003 Statacorp, 2001, STAT STAT SOFTW REL Williams J, 2005, AUTISM, V9, P45, DOI 10.1177/136261305049029 NR 12 TC 24 Z9 25 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUL PY 2006 VL 10 IS 4 BP 415 EP 427 DI 10.1177/1362361306066612 PG 13 WC Psychology, Developmental SC Psychology GA 068RA UT WOS:000239390900009 PM 16908483 ER PT J AU Ferreri, SJ Tamm, L Wier, KG AF Ferreri, SJ Tamm, L Wier, KG TI Using food aversion to decrease severe pica by a child with autism SO BEHAVIOR MODIFICATION LA English DT Article DE pica; food aversion; autism ID OVERCORRECTION AB Food aversion was shown to be effective in the reduction of plastic pica by a 4-year-old boy with autism. The participant was suffering from digestive complications due to the ingestion of plastic from a variety of toys. The intervention was initially conducted in the child's preschool classroom during instructional periods and was systematically generalized to the entire preschool classroom, and eventually to both classrooms within the preschool and across 25 teachers. The success of the intervention in decreasing pica was enhanced by its achievement in not reducing interactions with toys, considering appropriate play skills were a target goal. C1 Ohio State Univ, Special Educ & Appl Behav Anal Doctoral Program, Columbus, OH 43210 USA. RP Ferreri, SJ (reprint author), Ohio State Univ, Special Educ & Appl Behav Anal Doctoral Program, Columbus, OH 43210 USA. 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PD JUL PY 2006 VL 30 IS 4 BP 456 EP 471 DI 10.1177/0145445504272970 PG 16 WC Psychology, Clinical SC Psychology GA 053EV UT WOS:000238289300005 PM 16723425 ER PT J AU Tarbox, RSF Ghezzi, PM Wilson, G AF Tarbox, Rachel S. F. Ghezzi, Patrick M. Wilson, Ginger TI The effects of token reinforcement on attending in a young child with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article ID HYPERACTIVE-CHILDREN; FIXED-RATIO; ECONOMY; SCHEDULES; BEHAVIOR AB The benefits of token economies have been widely established, however there are very few empirical studies on the effects of token reinforcement on the behavior of young children with autism. The establishment of conditioned reinforcers such as tokens may be important in interventions for children with autism. Token reinforcement was used to increase the attending behavior of a young child with autism during discrete trials instruction for academic and communication skills. A reversal design showed that token reinforcement sustained attending only when the back-up reinforcer was available and was accessed immediately. The results extend and corroborate findings on token reinforcement reported in other applied settings and are also consistent with findings from basic research on conditioned reinforcement. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Ctr Autism & Related Disorders Inc, Tarzana, CA 91356 USA. Univ Nevada, Reno, NV 89557 USA. RP Tarbox, RSF (reprint author), Ctr Autism & Related Disorders Inc, 19019 Ventura Blvd, Tarzana, CA 91356 USA. EM r.tarbox@centerforautism.com CR Adamson L. B., 1995, JOINT ATTENTION ITS, P205 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERSON SR, 1996, BEHAV INTERVENTION Y AYLLON T, 1975, J APPL BEHAV ANAL, V8, P137, DOI 10.1901/jaba.1975.8-137 Ayllon T., 1968, TOKEN EC MOTIVATIONA AYLLON T, 1965, J EXP ANAL BEHAV, V8, P357, DOI 10.1901/jeab.1965.8-357 Bijou S. 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PD JUL PY 2006 VL 21 IS 3 BP 155 EP 164 DI 10.1002/bin.213 PG 10 WC Psychology, Clinical SC Psychology GA 068CG UT WOS:000239348800001 ER PT J AU Arntzen, E Tonnessen, IR Brouwer, G AF Arntzen, Erik Tonnessen, Ingvil Ro Brouwer, Grete TI Reducing aberrant verbal behavior by building a repertoire of rational verbal behavior SO BEHAVIORAL INTERVENTIONS LA English DT Article; Proceedings Paper CT ABA Convention 2004 CY 2004 CL Boston, MA SP ABA ID FUNCTIONAL-ANALYSIS; BIZARRE SPEECH; PSYCHOTIC SPEECH; REINFORCEMENT; SCHIZOPHRENIA; CHILD AB The purpose of the present study was to train different verbal classes in a 44-year-old woman to reduce aberrant verbal behavior. She had been hospitalized for 22 years in different psychiatric institutions, and has been diagnosed with schizophrenia, developmental disabilities, non-organic psychosis, and autism. Assessment of her verbal behavior showed that a small amount was adequate verbal behavior, whereas almost the entire repertoire of verbal behavior could be characterized as aberrant verbal behavior ('psychotic' and repetitive verbal behavior), and this behavior was maintained by social reinforcement such as smiles, various comments from other persons. The treatment program was based on results from the assessment results and was focused on establishing relationships between a variety of verbal response responses and proper controlling variables. She was trained to produce different verbal classes, mainly mand, tact, intraverbal, textual, transcription, and dictation responses. The duration of aberrant verbal behavior and the rate of 'Psychotic' verbal behavior were gradually reduced as a function of an increasing number of adequate verbal responses. In the study, we present data covering a very long period; the last data point was acquired 25 months after the start of the program. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Akershus Univ Coll, N-2001 Lillestrom, Norway. Community Based Serv, Kristiansand, Norway. RP Arntzen, E (reprint author), Akershus Univ Coll, POB 423, N-2001 Lillestrom, Norway. EM erik.arntzen@equivalence.net CR AYLLON T, 1959, J EXP ANAL BEHAV, V2, P323, DOI 10.1901/jeab.1959.2-323 BAER DM, 1968, J APPL BEHAV ANAL, V1, P91, DOI 10.1901/jaba.1968.1-91 BARTLETT D, 1971, J BEHAV THER EXP PSY, V2, P145, DOI 10.1016/0005-7916(71)90031-0 Catania A. 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Edrisinha, Chaturi Sigafoos, Jeff Lancioni, Giulio Andrews, Alonzo TI Isolating the evocative and abative effects of an establishing operation on challenging behavior SO BEHAVIORAL INTERVENTIONS LA English DT Article ID SELF-INJURY; FUNCTIONAL-ANALYSIS; SLEEP-DEPRIVATION; INTERVENTION; ASSESSMENTS; REFINEMENTS; AGGRESSION; ATTENTION; ESCAPE AB Establishing operations (EO) influence operant responding by altering the reinforcing effectiveness of consequences (reinforcer establishing or abolishing effect) and changing the frequency of behavior that has been reinforced by those consequences in the past (evocative or abative effect) (Michael, 1982, 1993). In this study we attempted to isolate the evocative and abative effects of an EO for positively reinforced challenging behavior with a person with autism and developmental disabilities. The study consisted of three phases. First, an analogue functional analysis identified attention as maintaining challenging behavior. Second, access to attention was systematically controlled (continuous access versus no access) immediately prior to functional analysis sessions in which the participant received attention on an FR1 schedule. Results of this phase indicated that challenging behavior occurred at higher levels during the functional analysis sessions when access to attention was restricted immediately prior to sessions (i.e., no access appeared to function as an EO). In the third phase, prior access to attention was again controlled as in the second phase of the study, however the participant was then placed on extinction. The results of this final phase seem to indicate that no access to the reinforcer prior to extinction had an evocative effect (produced high levels of responding) whereas access to the reinforcer had an abative effect (produced lower levels of responding) during extinction sessions. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Univ Texas, Dept Special Educ, Austin, TX 78712 USA. 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PD JUL PY 2006 VL 21 IS 3 BP 195 EP 204 DI 10.1002/bin.215 PG 10 WC Psychology, Clinical SC Psychology GA 068CG UT WOS:000239348800004 ER PT J AU Anderson, S Morris, J AF Anderson, Stephen Morris, Jane TI Cognitive behaviour therapy for people with Asperger syndrome SO BEHAVIOURAL AND COGNITIVE PSYCHOTHERAPY LA English DT Article DE Asperger syndrome; cognitive behaviour therapy ID RANDOMIZED CONTROLLED-TRIAL; HIGH-FUNCTIONING ADULTS; LIFELONG ECCENTRICITY; SOCIAL-ISOLATION; PRIMARY-CARE; AUTISM; DISORDERS; MIND; DEPRESSION; ANXIETY AB People with Asperger syndrome (AS) appear to have higher than expected rates of co-morbid psychiatric disorder. The main co-morbid diagnoses are anxiety disorders and depression, but eating disorders, obsessive compulsive disorder, substance abuse and bipolar affective disorder have all been reported. Cognitive Behaviour Therapy (CBT) is used effectively to treat these conditions, so could it be used in people who also have Asperger syndrome? This paper reviews important components and characteristics of cognitive behaviour therapy in relation to its use with people who have Asperger syndrome with reference to the relevant literature and to feedback from people with AS. The use of CBT in people with Asperger syndrome appears promising, but further work is needed to evaluate its effectiveness and to examine which particular aspects of therapy are helpful. C1 Learning Disabil Serv, Lothian Primary Care, Edinburgh EH10 5NQ, Midlothian, Scotland. RP Anderson, S (reprint author), Learning Disabil Serv, Lothian Primary Care, 65 Morningside Dr, Edinburgh EH10 5NQ, Midlothian, Scotland. 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PD JUL PY 2006 VL 34 IS 3 BP 293 EP 303 DI 10.1017/S1352465805002651 PG 11 WC Psychology, Clinical SC Psychology GA 070FC UT WOS:000239504700004 ER PT J AU Edwards, MJ AF Edwards, Marshall J. TI Review: Hyperthermia and fever during pregnancy SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY LA English DT Review DE hyperthermia; influenza; fever; pregnancy; prenatal death; birth defects; behavioral problems ID NEURAL-TUBE DEFECTS; PRENATAL HEAT-STRESS; POSTIMPLANTATION RAT EMBRYOS; MATURE GUINEA-PIGS; IN-UTERO EXPOSURE; MATERNAL HYPERTHERMIA; BRAIN GROWTH; GESTATIONAL HYPERTHERMIA; CONGENITAL DEFECTS; FEBRILE ILLNESSES AB An episode of hyperthermia is not uncommon during pregnancy. The consequences depend on the extent of temperature elevation, its duration, and the stage of development when it occurs. Mild exposures during the preimplantation period and more severe exposures during embryonic and fetal development often result in prenatal death and abortion. Hyperthermia also causes a wide range of structural and functional defects. The central nervous system (CNS) is most at risk probably because it cannot compensate for the loss of prospective neurons by additional divisions by the surviving neuroblasts and it remains at risk at stages throughout pre- and postnatal life. In experimental animals the most common defects are of the neural tube, microphthalmia, cataract, and micrencephaly, with associated functional and behavioral problems. Defects of craniofacial development including clefts, the axial and appendicular skeleton, the body wall, teeth, and heart are also commonly found. Nearly all these defects have been found in human epidemiological studies following maternal fever or hyperthermia during pregnancy. Suggested future human studies include problems of CNS function after exposure to influenza and fever, including mental retardation, schizophrenia, autism, and cerebral palsy. 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Their performance was compared with that of 8 autistics without a visuospatial peak (HFA-NP), 10 typically developing individuals (TD) and 8 gifted comparison participants with a visuospatial peak (TD-P). Both HFA-P and HFA-NP groups presented with diminished detrimental influence of increasing perceptual coherence compared with their BDT-matched comparison groups. Neither autistic group displayed a deficit in construction of global representations. The HFA-P group showed no differences in performance level or profile in comparison with the gifted BDT-matched [i.e. higher full-scale IQ (FSIQ)] group, apart from locally oriented perception. Diminished detrimental influence of perceptual coherence on BDT performance is both sensitive and specific to autism, and superior low-level processing interacts with locally oriented bias to produce outstanding BDT performance in a subgroup of autistic individuals. 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SO BRAIN & DEVELOPMENT LA English DT Article DE attention-deficit/hyperactivity disorder; pervasive development disorders ID SPECTRUM DISORDERS; COMORBIDITY; CHILDREN; AUTISM AB We studied the relationship between patients with attention-deficit/hyperactivity disorder (ADHD) and those with pervasive developmental disorders (PDD), using the High-Functioning Autism Spectrum Screening Questionnaire (ASSQ) and ADHD Rating Scale-IV. The ASSQ scores of the PDD group and the ADHD group were significantly higher than the control group. Furthermore, the PDD group scored higher than the ADHD group. Both groups also showed higher scores than the control group in all three domains, that is, restricted and repetitive behavior, social interaction, and communication problem. The PDD and the ADHD group showed no significant difference in the domains of communication problem, and restricted and repetitive behavior. 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D., 2000, CHILDRENS REASONING, P169 NR 43 TC 64 Z9 65 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0009-3920 J9 CHILD DEV JI Child Dev. PD JUL-AUG PY 2006 VL 77 IS 4 BP 1034 EP 1049 DI 10.1111/j.1467-8624.2006.00917.x PG 16 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 066UU UT WOS:000239256400014 PM 16942504 ER PT J AU Maughan, B Carroll, J AF Maughan, Barbara Carroll, Julia TI Literacy and mental disorders SO CURRENT OPINION IN PSYCHIATRY LA English DT Article DE comorbidity; dyslexia; mental disorders ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY DISORDER; READING-DISABILITY; COMORBIDITY; DYSLEXIA; CHILDREN; ACHIEVEMENT; HYPERLEXIA; CHILDHOOD; PRESCHOOL AB This review examines recent evidence on the comorbidity between literacy problems and psychiatric disorder in childhood and,discusses possible contributory factors. Recent studies confirm the substantial overlap of literacy problems with a range of emotional/behavioural difficulties in childhood. Literacy problems and inattention may share genetic influences, contributing to associations with attention deficit hyperactivity disorder. To an extent; links with conduct problems may be also mediated by attentional difficulties. In addition, findings suggest bidirectional influences whereby disruptive behaviours impede reading progress and reading failure exacerbates risk for behaviour problems. Associations between literacy problems and anxiety disorders are not entirely mediated by inattentiveness. Rather, comorbid anxiety disorders seem likely to arise from the stressors associated with reading failure. Findings in relation to depression are less consistent, but suggest that poor readers may be vulnerable to low mood. Children with autism seem more likely to face problems in reading comprehension than the decoding difficulties more prominent in other disorders. Literacy problems are associated with increased risks of both externalizing and internalizing disorders in childhood, with different mechanisms likely to be implicated in each case. When comorbid problems occur, each is likely to require separate treatment. C1 Kings Coll, Inst Psychiat, MRC, Social Genet & Dev Psychiat Ctr, London SE5 8AF, England. Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. RP Maughan, B (reprint author), Kings Coll, Inst Psychiat, MRC, Social Genet & Dev Psychiat Ctr, Box PO46, London SE5 8AF, England. 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Opin. Psychiatr. PD JUL PY 2006 VL 19 IS 4 BP 350 EP 354 DI 10.1097/01.yco.0000228752.79990.41 PG 5 WC Psychiatry SC Psychiatry GA 060KM UT WOS:000238801100002 PM 16721162 ER PT J AU Volkmar, FR Wiesner, LA Westphal, A AF Volkmar, Fred R. Wiesner, Lisa A. Westphal, Alexander TI Healthcare issues for children on the autism spectrum SO CURRENT OPINION IN PSYCHIATRY LA English DT Article DE autism; healthcare; measles-mumps-rubella vaccine; screening ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME; YOUNG-CHILDREN; ASSOCIATION; MEASLES; RISPERIDONE; VACCINE; MUMPS; TRIAL; NEEDS AB We provide a summary of issues relevant to healthcare and health delivery in autism and related disorders, with a focus on work published in the past 5 years. Autism has a strong genetic basis as evidenced by the high recurrence rate in families and its associations with Fragile X syndrome and tuberous sclerosis. Early diagnosis of autism is important, given the potential for improvement with intervention. Although its associations have been reported with events such as measles-mumps-rubella immunization, large-scale studies have not supported, such links. Controlled drug trials have increased in frequency and drug treatment may be helpful in addressing frequently associated behavioural and emotional difficulties. Alternative treatments are frequently preferred by parents. Knowledge of autism among healthcare professionals has increased but gaps remain. Physicians and other professionals can facilitate the delivery of healthcare services to individuals with autism. Awareness of empirically validated treatments will facilitate work with individuals with autism and related disorders as well as with their families. C1 Yale Univ, Sch Med, New Haven, CT 06520 USA. RP Volkmar, FR (reprint author), POB 207900, New Haven, CT 06520 USA. 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Opin. Psychiatr. PD JUL PY 2006 VL 19 IS 4 BP 361 EP 366 DI 10.1097/01.yco.0000228754.64743.66 PG 6 WC Psychiatry SC Psychiatry GA 060KM UT WOS:000238801100004 PM 16721164 ER PT J AU Baird, G Robinson, RO Boyd, S Charman, T AF Baird, Gillian Robinson, Richard O. Boyd, Stuart Charman, Tony TI Sleep electroencephalograms in young children with autism with and without regression SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; LANDAU-KLEFFNER-SYNDROME; SLOW-WAVE SLEEP; SPECTRUM DISORDERS; EEG ABNORMALITIES; COGNITIVE IMPAIRMENT; LANGUAGE REGRESSION; CHILDHOOD; SEIZURES; EPILEPSY AB A link has been postulated between regressive autism and the spectrum of epileptic encephalopathic conditions including Landau-Kleffner syndrome with the suggestion that subclinical epilepsy may be causative of regression in autism. This is an audit of investigation using sleep electroencephalograms (EEG) in 64 children (56 males, 8 females; mean age 35.6mo [SD 8.2mo]; range 18-48mo) with autism. No child had a history suggestive of epilepsy. Thirty-nine of the children presented with regressive autism and 20 of the participants showed some epileptiform abnormality. There was no significant difference in epileptiform activities in those who showed regression compared with those who did not. No child showed electrical status epilepticus with continuous spike-wave discharges in slow sleep. There was no evidence that these cases of autism with and without regression were associated with epileptic encephalopathy. The significance of epileptiform discharges without epilepsy in the sleep EEG in autism remains unknown. C1 Guys Hosp, Newcomen Ctr, London SE1 9RT, England. Great Ormond St Hosp Sick Children, London WC1N 3JH, England. UCL, Inst Child Hlth, Behav & Sci Unit, London, England. RP Baird, G (reprint author), Guys Hosp, Newcomen Ctr, St Thomas St, London SE1 9RT, England. EM Gillian.Baird@gstt.sthames.nhs.uk RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR ADRIEN JL, 1991, J AUTISM DEV DISORD, V21, P43, DOI 10.1007/BF02206996 Aldenkamp AP, 2004, EPILEPSY BEHAV, V5, pS25, DOI 10.1016/j.yebeh.2003.11.005 BAILEY A, 1995, PSYCHOL MED, V25, P63 Beun AM, 1998, ELECTROEN CLIN NEURO, V106, P44, DOI 10.1016/S0013-4694(97)00083-7 Binnie C, 2001, EPILEPSY RES, V45, P7, DOI 10.1016/S0920-1211(01)00204-2 Binnie CD, 2003, LANCET NEUROL, V2, P725, DOI 10.1016/S1474-4422(03)00584-2 Canitano R, 2005, J CHILD NEUROL, V20, P27, DOI 10.1177/08830738050200010401 Chez MG, 2004, EPILEPSY BEHAV, V5, P159, DOI 10.1016/j.yebeh.2003.11.019 Clark RJH, 2002, CR CHIM, V5, P7, DOI 10.1016/S1631-0748(02)01341-3 Clarke Dave F., 2002, Epilepsia, V43, P79 Danielsson S, 2005, EPILEPSIA, V46, P918, DOI 10.1111/j.1528-1167.2005.57504.x Filipek PA, 2000, NEUROLOGY, V55, P468 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Green H., 2005, MENTAL HLTH CHILDREN Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Hrdlicka M, 2004, EUR CHILD ADOLES PSY, V13, P209, DOI 10.1007/s00787-004-0353-7 Hughes JR, 2005, CLIN EEG NEUROSCI, V36, P15 Kagan-Kushnir T, 2005, J CHILD NEUROL, V20, P197 Kallen RJ, 2001, PEDIATRICS, V107, P1232, DOI 10.1542/peds.107.5.1232 Kielinen M, 2004, AUTISM, V8, P49, DOI 10.1177/1362361304040638 Kim HL, 2006, EPILEPSIA, V47, P394, DOI 10.1111/j.1528-1167.2006.00434.x KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 Leiter R. 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Med. Child Neurol. PD JUL PY 2006 VL 48 IS 7 BP 604 EP 608 DI 10.1017/S0012162206001265 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 064ZB UT WOS:000239128100013 PM 16780632 ER PT J AU Humphrey, A Neville, BGR Clarke, A Bolton, PF AF Humphrey, Ayla Neville, Brian G. R. Clarke, Antonia Bolton, Patrick F. TI Autistic regression associated with seizure onset in an infant with tuberous sclerosis SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article AB We report here on a male diagnosed with tuberous sclerosis at 6 months of age. The child was treated with vigabatrin at age 6 months after an abnormal electroencephalogram but before onset of seizures. Vigabatrin was discontinued at age 13 months to avoid possible visual field defects. At 21 months, the child developed partial seizures with secondary generalization and infantile spasms. Standardized developmental assessments were performed at 12, 18, 24, 30, and 36 months of age. Cognitive and social development were normal until age 21 months and the onset of seizures. When assessed at 24 months, the child met criteria for autism and learning disability.* This case indicates that the onset of epilepsy during an early stage in brain development can be associated with autistic regression and persistent developmental disorder. The case suggests the need to consider if possible visual field defects with vigabatrin outweigh the potentially deleterious effects of uncontrolled seizures. C1 Univ Cambridge, Dev Psychiat Sect, Cambridge CB2 2AH, England. UCL, Inst Child Hlth, Neurosci Unit, London, England. Great Ormond St Hosp Children NHS Trust, London WC1N 3JH, England. St George Hosp, London, England. Kings Coll, Dept Psychiat, Inst Psychiat, London WC2R 2LS, England. Kings Coll, MRC Ctr Social Genet & Dev Psychiat, Inst Psychiat, London WC2R 2LS, England. RP Humphrey, A (reprint author), Univ Cambridge, Dev Psychiat Sect, Douglas House,18b Trumpington Rd, Cambridge CB2 2AH, England. EM ah290@cam.ac.uk RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 CR *AM GUID SERV, 1995, MULL SCAL EARL LEARN American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bolton PF, 2002, BRAIN, V125, P1247, DOI 10.1093/brain/awf124 DEONNA T, 1993, DEV MED CHILD NEUROL, V35, P158 Gomez M. R., 1999, TUBEROUS SCLEROSIS C Humphrey A, 2004, EUR CHILD ADOLES PSY, V13, P159, DOI 10.1007/s00787-004-0383-1 Jambaque I, 2000, EPILEPSY RES, V38, P151, DOI 10.1016/S0920-1211(99)00082-0 Lord C., 1999, AUTISM DIAGNOSTIC OB World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 9 TC 29 Z9 29 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD JUL PY 2006 VL 48 IS 7 BP 609 EP 611 DI 10.1017/S0012162206001277 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 064ZB UT WOS:000239128100014 PM 16780633 ER PT J AU Hertz-Picciotto, I Croen, LA Hansen, R Jones, CR van de Water, J Pessah, IN AF Hertz-Picciotto, Irva Croen, Lisa A. Hansen, Robin Jones, Carrie R. van de Water, Judy Pessah, Isaac N. TI The CHARGE study: An epidemiologic investigation of genetic and environmental factors contributing to autism SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE autism; autistic spectrum disorder; developmental delay; environment; genetics; mental retardation; pervasive developmental disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; FETAL VALPROATE SYNDROME; SPECTRUM DISORDER; INFANTILE-AUTISM; CONGENITAL CYTOMEGALOVIRUS; FAMILIAL AGGREGATION; DIAGNOSTIC INTERVIEW; CHANGING PREVALENCE; TUBEROUS SCLEROSIS; BRAIN AB Causes and contributing factors for autism are poorly understood. Evidence suggests that prevalence is rising, but the extent to which diagnostic changes and improvements in ascertainment contribute to this increase is unclear. Both genetic and environmental factors are likely to contribute etiologically. Evidence from twin, family, and genetic studies supports a role for an inherited predisposition to the development of autism. Nonetheless, clinical, neuroanatomic, neurophysiologic, and epidemiologic studies suggest that gene penetrance and expression may be influenced, in some cases strongly, by the prenatal and early postnatal environmental milieu. Sporadic studies link autism to xenobiotic chemicals and/or viruses, but few methodologically rigorous investigations have been undertaken. In light of major gaps in understanding of autism, a large case-control investigation of underlying environmental and genetic causes for autism and triggers of regression has been launched. The CHARGE (Childhood Autism Risks from Genetics and Environment) study will address a wide spectrum of chemical and biologic exposures, susceptibility factors, and their interactions. Phenotypic variation among children with autism will be explored, as will similarities and differences with developmental delay. The CHARGE study infrastructure includes detailed developmental assessments, medical information, questionnaire data, and biologic specimens. The CHARGE study is linked to University of California-Davis Center for Children's Environmental Health laboratories in immunology, xenobiotic measurement, cell signaling, genomics, and proteomics. The goals, study design, and data collection protocols are described, as well as preliminary demographic data on study participants and on diagnoses of those recruited through the California Department of Developmental Services Regional Center System. C1 Univ Calif Davis, Dept Publ Hlth Sci, Sch Med, Div Epidemiol, Davis, CA 95616 USA. Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. Kaiser Permanente, Kaiser Fdn, Res Inst, Div Res, Oakland, CA USA. Univ Calif Davis, Dept Pediat, Sch Med, Davis, CA 95616 USA. Univ Calif Davis, Dept RheumatolAllergy & Clin Immunol, Sch Med, Davis, CA 95616 USA. Univ Calif Davis, Dept Mol Biosci, Sch Vet Med, Davis, CA 95616 USA. RP Hertz-Picciotto, I (reprint author), Univ Calif Davis, Dept Publ Hlth Sci, Sch Med, Div Epidemiol, TB 168, Davis, CA 95616 USA. 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Med. Res. PD JUL PY 2006 VL 124 IS 1 BP 5 EP 8 PG 4 WC Immunology; Medicine, General & Internal; Medicine, Research & Experimental SC Immunology; General & Internal Medicine; Research & Experimental Medicine GA 085AG UT WOS:000240574900002 ER PT J AU Naito, M Koyama, K AF Naito, Mika Koyama, Kayo TI The development of false-belief understanding in Japanese children: Delay and difference? SO INTERNATIONAL JOURNAL OF BEHAVIORAL DEVELOPMENT LA English DT Article DE behavioral and situational explanations; false belief; interdependent and independent cultures; interpersonal transfer tasks; Japanese children; mental states ID SOCIAL EXPLANATION; PRESCHOOL-CHILDREN; MIND; EMOTION; CULTURE; SELF; LANGUAGE; AUTISM; DESIRE; TASKS AB Three experiments investigated the development of Japanese children's false-belief understanding. In Experiment 1, children's mastery of two standard false-belief tasks was considerably later and slower than typically reported, with the full development between 6 and 7 years. Experiments 2 and 3 tested Japanese 6- to 8-year-olds on interpersonal transfer tasks where a relocated item was a person who changed locations with and without their own intention. Children's judgments on the main character's belief about this person's whereabouts were not influenced by the protagonists' different mental states included in the tasks; children's justifications referred not to the people's belief or desire but primarily to their behaviors and social rules. Results suggest that Japanese children show not only a delay in false-belief understanding but a cultural difference in reasoning about human action as attributing it to behavioral and situational cues, rather than to individuals' mental states. C1 Joetsu Univ Educ, Dept Sch Educ, Joetsu 9438512, Japan. 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Lindsay, Geoff Letchford, Becky Mackie, Clare TI Educational provision for children with specific speech and language difficulties: perspectives of speech and language therapy service managers SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE children; provision; speech and language therapy; UK; services; mainstream speech and language difficulties; interventions ID IMPAIRMENT; AUTISM; DIFFERENTIATE; DISORDER; WORKING; SLI AB Background: Children with specific speech and language difficulties (SSLD) pose a challenge to the education system, and to speech and language therapists who support them, as a result of their language needs and associated educational and social-behavioural difficulties. The development of inclusion raises questions regarding appropriate provision, whether the tradition of language units or full inclusion into mainstream schools. Aims: To gather the views of speech and language therapy service managers in England and Wales regarding approaches to service delivery, terminology and decision-making for educational provision, and the use of direct and indirect (consultancy) models of intervention. Method & Procedures: The study reports on a national survey of speech and language therapy (SLT) services in England and Wales (129 respondents, 72.1% response rate) and interviews with 39 SLT service managers. Outcomes & Results: Provision varied by age group with support to children in the mainstream common from pre-school to the end of Key Stage 2 (up to 11 years), and to those in designated specialist provision, common at Key Stages 1/2 (ages 5-11 years), but less prevalent at Key Stages 3/4 (11-16 years). Decision-making regarding provision was influenced by the lack of common terminology, with SSLD and specific language impairment (SLI) the most common, and criteria, including the use of the discrepancy model for defining SSLD. Practice was influenced by the difficulties in distinguishing children with SSLD from those with autistic spectrum disorder, and difficulties translating policies into practice. Conclusions: The implications of the study are discussed with reference to SLT practice, including consultancy models, and the increasingly prevalent policy in local education authorities of inclusion of children with special educational needs. C1 Univ London, Inst Educ, London WC1, England. Univ Warwick, CEDAR, Coventry CV4 7AL, W Midlands, England. RP Dockrell, JE (reprint author), Univ London, Inst Educ, London WC1, England. 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J. Lang. Commun. Disord. PD JUL-AUG PY 2006 VL 41 IS 4 BP 423 EP 440 DI 10.1080/13682820500442073 PG 18 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 072DX UT WOS:000239654100006 PM 16815810 ER PT J AU Cook, EH AF Cook, E. H. TI Autism: Genetics SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL USA. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S19 EP S20 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500074 ER PT J AU Court, JA Perry, EK AF Court, J. A. Perry, E. K. TI Neurochemical pathological studies of autism SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Univ Newcastle, Inst Ageing & Hlth, Newcastle Upon Tyne, Tyne & Wear, England. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S19 EP S19 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500073 ER PT J AU Dhossche, D Shah, A Wing, L AF Dhossche, D. Shah, A. Wing, L. TI Catatonia in autism: A treatable syndrome? SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Univ Mississippi, Med Ctr, University, MS 38677 USA. Ctr Social & Commun Disorders, Bromley, Kent, England. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S262 EP S262 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495501413 ER PT J AU Clark, LL AF Clark, Louise L. TI Intellectual impairment: a forgotten speciality SO INTERNATIONAL JOURNAL OF NURSING STUDIES LA English DT Editorial Material DE intellectual impairment; diagnostic issues; expertise; autism; education ID LEARNING-DISABILITIES; ADULTS; PEOPLE; SERVICES; ILLNESS; AUTISM C1 Kings Coll, Florence Nightingale Sch Nursing & Midwifery, London WC2R 2LS, England. RP Clark, LL (reprint author), Kings Coll, Florence Nightingale Sch Nursing & Midwifery, Waterloo Rd, London WC2R 2LS, England. EM louise.l.clark@kcl.ac.uk CR Carnaby S, 1998, J INTELLECT DEV DIS, V23, P219, DOI 10.1080/13668259800033711 Chaplin R, 2004, J INTELL DISABIL RES, V48, P1, DOI 10.1111/j.1365-2788.2004.00580.x Deb S, 2001, J INTELL DISABIL RES, V45, P495 Department of Health, 2001, VAL PEOPL NEW STRAT Doody GA, 1998, BRIT J PSYCHIAT, V173, P145, DOI 10.1192/bjp.173.2.145 Filipek PA, 2000, NEUROLOGY, V55, P468 Gilbert T, 2003, INT J NURS STUD, V40, P781, DOI 10.1016/S0020-7489(03)00115-9 Jick H, 2003, PHARMACOTHERAPY, V23, P1524, DOI 10.1592/phco.23.15.1524.31955 Mawle E, 2006, INT J NURS STUD, V43, P623, DOI 10.1016/j.ijnurstu.2005.11.011 Mencap, 2004, TREAT ME RIGHT BETT Moore G, 2003, INT J NURS STUD, V40, P771, DOI 10.1016/S0020-7489(03)00111-1 Slevin E, 2005, INT J NURS STUD, V42, P415, DOI 10.1016/j.ijnurstu.2004.09.020 Xenitidis K, 2004, J INTELL DISABIL RES, V48, P11, DOI 10.1111/j.1365-2788.2004.00586.x NR 13 TC 2 Z9 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0020-7489 J9 INT J NURS STUD JI Int. J. Nurs. Stud. PD JUL PY 2006 VL 43 IS 5 BP 525 EP 526 DI 10.1016/j.ijnurstu.2006.03.007 PG 2 WC Nursing SC Nursing GA 062TJ UT WOS:000238967200001 PM 16690061 ER PT J AU Mawle, E Griffiths, P AF Mawle, Elizabeth Griffiths, Peter TI Screening for autism in pre-school children in primary care: Systematic review of English Language tools SO INTERNATIONAL JOURNAL OF NURSING STUDIES LA English DT Review DE autistic disorder; sensitivity and specificity; infant; child; pre-school; mass screening; primary health care (all MESH) ID DIAGNOSTIC OBSERVATION SCHEDULE; PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIORAL SUMMARIZED EVALUATION; RATING-SCALE; CHILDHOOD AUTISM; MENTAL-RETARDATION; YOUNG-CHILDREN; PEDIATRICIANS ROLE; SPECTRUM DISORDER; TOKYO VERSION AB Objectives: To review the accuracy of brief screening tools for autism in pre-school children. Design: Systematic review of diagnostic accuracy studies. Data sources: Medline, Embase, Cinahl and Psychlit plus references of identified papers and contact with authors. Subjects: Children and infants aged 5 years or less without a prior diagnosis of autism or pervasive development delay. Interventions: Tools/checklists appropriate for use in screening for autism in primary care settings. Outcome measures: Sensitivity, specificity, positive and negative predictive value of screening tools and likelihood ratios relative to a diagnostic assessment made using either DSM-III/IV or ICD 10 diagnosis. Results: Three studies considering two tools were identified. The CHecklist for Autism in Toddlers (CHAT) was tested on an appropriate population sample with moderate long-term follow-up but demonstrated poor sensitivity and positive predictive value. Weaker evidence suggested that the Modified CHecklist for Autism in Toddlers (M-CHAT) had high sensitivity but follow-up was of shorter term and less comprehensive. Conclusions: The CHAT demonstrated a level of sensitivity unlikely to be useful for population screening purposes, however, its high specificity suggests it has utility in secondary screening. The M-CHAT is a parent only report and might be more sensitive, and therefore appropriate for population screening. However, full conclusions regarding its accuracy cannot be drawn until follow-up data has been collected. (c) 2005 Elsevier Ltd. All rights reserved. C1 Kings Coll, Florence Nightingale Sch Nursing & Midwifery, London SE1 8WA, England. Westminster Primary Care Trust, London SE24 0AH, England. RP Griffiths, P (reprint author), Kings Coll, Florence Nightingale Sch Nursing & Midwifery, Waterloo Rd, London SE1 8WA, England. 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J. Nurs. Stud. PD JUL PY 2006 VL 43 IS 5 BP 623 EP 636 DI 10.1016/j.ijnurstu.2005.11.011 PG 14 WC Nursing SC Nursing GA 062TJ UT WOS:000238967200011 PM 16387303 ER PT J AU Allik, H Larsson, JO Smedje, H AF Allik, Hiie Larsson, Jan-Olov Smedje, Hans TI Sleep patterns of school-age children with Asperger syndrome or high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE sleep; Asperger syndrome; high-functioning autism; actigraphy; sleep diary ID DISORDER; IDENTIFICATION; INTELLIGENCE; ADOLESCENTS; PREVALENCE AB Sleep patterns of 32 school-age children with Asperger syndrome (AS) and high-functioning autism (HFA) were compared to those of 32 typically developing age- and gender-matched children, using parent survey and one week of diary and actigraphic monitoring. Parents of children with AS/HFA more commonly reported that their children had difficulty falling asleep. One week of sleep recording with diary and actigraphy confirmed that children in the AS/HFA group spent a longer time awake in bed before falling asleep than children in the control group, possibly because the children in the AS/HFA group had earlier bedtimes. Other essential aspects of sleep patterns coincided between the groups. The sleep patterns of children with AS and HFA did not differ. C1 Astrid Lindgren Childrens Hosp, Karolinska Inst, Dept Woman & Child Hlth, Child & Adolescent Psychiat Unit, S-17176 Stockholm, Sweden. Uppsala Univ, Dept Neurosci, Uppsala, Sweden. RP Allik, H (reprint author), Astrid Lindgren Childrens Hosp, Karolinska Inst, Dept Woman & Child Hlth, Child & Adolescent Psychiat Unit, Q3,O4, S-17176 Stockholm, Sweden. EM hiie.allik@ki.se CR Acebo C, 1999, SLEEP, V22, P95 American Psychiatric Association, 1994, DIANG STAT MAN MENT Ancoli-Israel S, 2003, SLEEP, V26, P342 ANDERS TF, 1978, CHILD PSYCHIAT HUM D, V9, P56, DOI 10.1007/BF01463220 BERGERON C, 1997, SLEEP RES, V26, P541 Brown LW, 1996, CHILD ADOL PSYCH CL, V5, P701 Bryson S. 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J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 WHO, 1993, ICD 10 CLASS MENT BE World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 37 TC 46 Z9 46 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2006 VL 36 IS 5 BP 585 EP 595 DI 10.1007/s10803-006-0099-9 PG 11 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900002 PM 16617404 ER PT J AU Pan, CY Frey, GC AF Pan, Chien-Yu Frey, Georgia C. TI Physical activity patterns in youth with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE physical activity; autism; youth ID CHILDREN; ADOLESCENTS; SCHOOL; BEHAVIOR; AGE; EXERCISE; ADULTS AB The purpose of this study was to examine age-related physical activity patterns in youth with autism spectrum disorders (ASD). Thirty youth, aged 10-19 years, were divided into three groups: elementary (n=9), middle (n=9) and high (n=12) school. Participants wore an accelerometer and completed an activity questionnaire for seven consecutive days. The main findings were that (a) elementary youth are more active than the other groups, regardless type of day or time period, and (b) there are no consistent patterns in physical activity of youth with ASD according to day or time period. Findings emphasize that interventions for this population should address increasing extracurricular physical activity options during adolescence. C1 Indiana Univ, Dept Kinesiol, Bloomington, IN 47405 USA. Natl Kaohsiung Normal Univ, Dept Phys Educ, Kaohsiung, Taiwan. RP Frey, GC (reprint author), Indiana Univ, Dept Kinesiol, HPER 179,1025 E 7th St, Bloomington, IN 47405 USA. 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PD JUL PY 2006 VL 36 IS 5 BP 597 EP 606 DI 10.1007/s10803-006-0101-6 PG 10 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900003 PM 16652237 ER PT J AU Hardan, AY Keshavan, MS Sreedhar, S Vemulapalli, M Minshew, NJ AF Hardan, Antonio Y. Keshavan, Matcheri S. Sreedhar, Sucheta Vemulapalli, Mahduri Minshew, Nancy J. TI An MRI study of minor physical anomalies in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE physical anomalies; MRI; autism; inter-orbit distance ID DIAGNOSTIC INTERVIEW; BRAIN VOLUME; CHILDREN; ADULTS AB The objective of this investigation was to examine the existence of minor physical anomalies (MPA) in autism. The interorbital and interlens distances were measured on MRI scans obtained from a sample of 40 nonmentally retarded individuals with autism and 41 healthy controls. No differences were observed between the two groups on any measurements. However, when the analysis was conducted using a split median procedure, individuals with autism and either low FSIQ, PIQ, or VIQ had shorter interorbital distances when compared to controls. Hypotelorism is a MPA that may be present in a subgroup of individuals with autism. Additional research is warranted using large sample sizes with a wide range of intellectual functioning. C1 Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94024 USA. Univ Pittsburgh, Western Psychiat Inst & Clin, Sch Med, Pittsburgh, PA 15213 USA. Wayne State Univ, Sch Med, Dept Psychiat & Behav Sci, Detroit, MI USA. RP Hardan, AY (reprint author), Stanford Univ, Dept Psychiat & Behav Sci, 401 Quarry Rd, Stanford, CA 94024 USA. 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TI Motor signs distinguish children with high functioning autism and Asperger's syndrome from controls SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE coordination; dysrhythmia; overflow; gait; balance; motor speed ID DEFICIT-HYPERACTIVITY DISORDER; DIAGNOSTIC OBSERVATION SCHEDULE; CLUMSINESS; BEHAVIOR; COORDINATION; IMPAIRMENT; REGRESSION; MOVEMENT; ADHD; BOYS AB While many studies of motor control in autism have focused on specific motor signs, there has been a lack of research examining the complete range of subtle neuromotor signs. This study compared performance on a neurologic examination standardized for children (PANESS, Physical and Neurological Exam for Subtle Signs, Denckla [1974 Developmental Medicine and Child Neurology, 16(6), 729-741]) between a group of 40 boys aged 6-17 with autism and average range IQs and a group of 55 typically developing boys. The Autism group was shown to have significant impairment on several measures of motor control compared to the Control group. Regression analyses revealed that a model including four PANESS variables offered a high level of discrimination in distinguishing boys with high-functioning autism from controls. C1 Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Dept Neurol & Psychiat, Baltimore, MD 21218 USA. Georgia State Univ, Atlanta, GA 30303 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat, Kennedy Krieger Inst, Baltimore, MD USA. Johns Hopkins Univ, Sch Publ Hlth, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Dept Neurol, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Dept Pediat, Baltimore, MD USA. RP Mostofsky, SH (reprint author), Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Dept Neurol & Psychiat, 707 N Broadway,Ste 516, Baltimore, MD 21218 USA. EM mostofsky@kennedykrieger.org CR *APA, 1994, DIAGN STATMAN MENT D Bruininks R. 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Autism Dev. Disord. PD JUL PY 2006 VL 36 IS 5 BP 613 EP 621 DI 10.1007/s10803-006-0109-y PG 9 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900005 PM 16609826 ER PT J AU Dziobek, I Fleck, S Kalbe, E Rogers, K Hassenstab, J Brand, M Kessler, J Woike, JK Wolf, OT Convit, A AF Dziobek, Isabel Fleck, Stefan Kalbe, Elke Rogers, Kimberley Hassenstab, Jason Brand, Matthias Kessler, Josef Woike, Jan K. Wolf, Oliver T. Convit, Antonio TI Introducing MASC: A movie for the assessment of social cognition SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; theory of mind; mindreading; naturalistic test formats; emotion recognition ID HIGH-FUNCTIONING ADULTS; NORMALLY DEVELOPING-CHILDREN; ASPERGER-SYNDROME; REVISED VERSION; AUTISM; MIND; RECOGNITION; DISORDER; FACE; ADOLESCENTS AB In the present study we introduce a sensitive video-based test for the evaluation of subtle mindreading difficulties: the Movie for the Assessment of Social Cognition (MASC). This new mindreading tool involves watching a short film and answering questions referring to the actors' mental states. A group of adults with Asperger syndrome (n = 19) and well-matched control subjects (n = 20) were administered the MASC and three other mindreading tools as part of a broader neuropsychological testing session. Compared to control subjects, Asperger individuals exhibited marked and selective difficulties in social cognition. A Receiver Operating Characteristic (ROC) analysis for the mindreading tests identified the MASC as discriminating the diagnostic groups most accurately. Issues pertaining to the multidimensionality of the social cognition construct are discussed. C1 NYU, Sch Med, Ctr Brain Hlth, New York, NY 10016 USA. Univ Clin Cologne, Dept Neurol, Cologne, Germany. Univ Bielefeld, Dept Psychol, D-4800 Bielefeld, Germany. Univ Cologne, Dept Neurosci & Rehabil, Cologne, Germany. Univ Bielefeld, Dept Physiol Psychol, D-4800 Bielefeld, Germany. CUNY, Grad Ctr, Dept Psychol, New York, NY 10021 USA. Ruhr Univ Bochum, Dept Psychol Methodol, D-4630 Bochum, Germany. RP Dziobek, I (reprint author), NYU, Sch Med, Ctr Brain Hlth, New York, NY 10016 USA. EM dziobi01@med.nyu.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BARONCOHEN S, 1992, J CHILD PSYCHOL PSYC, V33, P1141, DOI 10.1111/j.1469-7610.1992.tb00934.x Baron-Cohen S, 1999, J AUTISM DEV DISORD, V29, P407, DOI 10.1023/A:1023035012436 BaronCohen S, 1997, VIS COGN, V4, P311, DOI 10.1080/713756761 Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x Brothers L., 1990, CONCEPTS NEUROSCIENC, V1, P27 Dyck MJ, 2001, EUR CHILD ADOLES PSY, V10, P105 EKMAN P, 1971, J PERS SOC PSYCHOL, V17, P124, DOI 10.1037/h0030377 Ekman P., 1999, HDB COGNITION EMOTIO FIELD S, 2001, DREHBUCHSCHREIBEN FR FLECK S, UNPUB MASCMC MOVIE A FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Grossman JB, 2000, J CHILD PSYCHOL PSYC, V41, P369, DOI 10.1017/S0021963099005466 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Happe FGE, 1998, DEV PSYCHOL, V34, P358, DOI 10.1037//0012-1649.34.2.358 HAPPE FGE, 1993, COGNITION, V48, P101, DOI 10.1016/0010-0277(93)90026-R Heavey L, 2000, J AUTISM DEV DISORD, V30, P225, DOI 10.1023/A:1005544518785 HOBSON RP, 1988, BRIT J PSYCHOL, V79, P441 Horn W., 1962, LEISTUNGSPRUFSYSTEM Howlin P, 2003, J AUTISM DEV DISORD, V33, P3, DOI 10.1023/A:1022270118899 HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 Jolliffe T, 1999, J AUTISM DEV DISORD, V29, P395, DOI 10.1023/A:1023082928366 Kaland N, 2002, J CHILD PSYCHOL PSYC, V43, P517, DOI 10.1111/1469-7610.00042 KALBE E, UNPUB TOO MUCH TOM S KALBE E, 2002, EXPT PSYCHOL Kleinman J, 2001, J AUTISM DEV DISORD, V31, P29, DOI 10.1023/A:1005657512379 Klin A., 1997, HDB AUTISM PERVASIVE, P94 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LOVELAND KA, 1995, DEV PSYCHOPATHOL, V7, P409 MACDONALD H, 1989, J CHILD PSYCHOL PSYC, V30, P865, DOI 10.1111/j.1469-7610.1989.tb00288.x Njiokiktjien C, 2001, EUR CHILD ADOLES PSY, V10, P79 Nunnally J. 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Autism Dev. Disord. PD JUL PY 2006 VL 36 IS 5 BP 623 EP 636 DI 10.1007/s10803-006-0107-0 PG 14 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900006 PM 16755332 ER PT J AU Hepburn, SL Stone, WL AF Hepburn, Susan L. Stone, Wendy L. TI Using Carey Temperament Scales to assess behavioral style in children with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE temperament; behavioral variability; assessment; autism ID FRAGILE-X-SYNDROME; PARENTS; STRESS AB Many researchers have suggested that temperament information could be useful for understanding the behavioral variability within the autism spectrum. The purpose of this brief report is to examine temperament profiles of 110 children with ASD (ages 3-8 years, 61 with Autistic Disorder, 42 with PDD-NOS; and 7 with Asperger Disorder) via a commonly used parent report measure of child temperament. Internal consistency of temperament dimensions, test-retest reliability, descriptions of means and standard deviations are examined, relative to previously published norms. Internal consistency of the dimensions and test-retest reliability were comparable to published norms; however, children with autism were rated as presenting with more extreme scores than typically-developing children on several dimensions. Limitations and implications for future work are discussed. C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Vanderbilt Childrens Hosp, Nashville, TN USA. RP Hepburn, SL (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Psychiat, 4200 E 9th Ave,Box C 268-21, Denver, CO 80262 USA. EM Susan.Hepburn@UCHSC.edu CR ANASTASI A, 1989, PUBLIC PERS MANAGE, V18, P471 Bailey DB, 2000, J AUTISM DEV DISORD, V30, P49 BAYDAR N, 1995, J APPL DEV PSYCHOL, V16, P339, DOI 10.1016/0193-3973(95)90024-1 Bristol M. M., 1984, SEVERELY HANDICAPPED, P91 CAMERON JR, 1978, AM J ORTHOPSYCHIAT, V48, P140 CAREY WB, 1986, TEMPERAMENT CLIN PRA, P239 Carey WB, 1995, CAREY TEMPERAMENT SC CAREY WB, 1989, CLIN ED APPL TEMPERA Chess S., 1996, TEMPERAMENT THEORY P CRONBACH LJ, 1951, PSYCHOMETRIKA, V16, P297 Dawson G, 2004, DEV PSYCHOL, V40, P271, DOI 10.1037/0012-1649.40.2.271 DILAVORE PC, 1991, THESIS U N CAROLINA EAVES LC, 1994, J AUTISM DEV DISORD, V24, P3, DOI 10.1007/BF02172209 Goldberg S., 1989, TEMPERAMENT CHILDHOO, P387 Hatton DD, 1999, DEV MED CHILD NEUROL, V41, P625, DOI 10.1017/S0012162299001280 HOLLANDER E, 2004, INT S S COND ANN M C HOLROYD J, 1976, AM J MENT DEF, V80, P431 Huck SW, 2000, READING STAT RES Kasari C, 1997, J AUTISM DEV DISORD, V27, P39, DOI 10.1023/A:1025869105208 KONSTANTAREAS MM, 1989, J CHILD PSYCHOL PSYC, V30, P459, DOI 10.1111/j.1469-7610.1989.tb00259.x KONSTANTAREAS MM, 2001, SOC RES CHILD DEV C LEIBOWITZ G, 1991, J DEV PHYS DISABIL, V3, P201, DOI 10.1007/BF01045976 MCDEVITT SC, 1978, J CHILD PSYCHOL PSYC, V19, P245, DOI 10.1111/j.1469-7610.1978.tb00467.x McDevitt SC, 1996, MANUAL BEHAV STYLE Q POLLACK CF, 1998, DISS ABSTR INT B, V59, P1 Rogers SJ, 2003, J AUTISM DEV DISORD, V33, P631, DOI 10.1023/B:JADD.0000006000.38991.a7 ROTHBART MK, 1999, DEV PERSPECTIVES CHI, P33 THOMAS A, 1968, TEMPERAMENT BEHAV DI Thomas A., 1963, BEHAV INDIVIDUALITY NR 29 TC 16 Z9 16 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2006 VL 36 IS 5 BP 637 EP 642 DI 10.1007/s10803-006-0110-5 PG 6 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900007 PM 16628481 ER PT J AU Whalen, C Schreibman, L Ingersoll, B AF Whalen, Christina Schreibman, Laura Ingersoll, Brooke TI The collateral effects of joint attention training on social initiations, positive affect, imitation, and spontaneous speech for young children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE joint attention; language; social skills; play; imitation ID DOWN-SYNDROME; LANGUAGE; COMMUNICATION; BEHAVIOR; PLAY AB Joint attention may be a core deficit in autism which underlies the abnormal development of later emerging social-communication behaviors. Given this theory, researchers have suggested that teaching young children with autism to engage in joint attention may lead to collateral increases in other non-targeted social-communication behaviors. In this study, children with autism participated in a 10-week joint attention training program and collateral changes in non-targeted behaviors were assessed. Following participation in the intervention, positive collateral changes were observed in social initiations, positive affect, imitation, play, and spontaneous speech. Results support the hypothesis that teaching joint attention skills leads to improvement in a variety of related skills and have implications for the treatment of young children with autism. C1 TeachTown Inc, Seattle, WA 98102 USA. Univ Washington, Autism Ctr, Seattle, WA 98195 USA. Univ Calif San Diego, Dept Psychol, San Diego, CA 92103 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Lewis & Clark Coll, Portland, OR 97219 USA. RP Whalen, C (reprint author), TeachTown Inc, 2815 Eastlake Ave E,Suite 300, Seattle, WA 98102 USA. EM chris@teachtown.com RI Ingersoll, Brooke/A-9117-2012 CR Adamson L. 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M., 1982, PROCEDURES MANUAL EA Sigman M, 1998, J CHILD PSYCHOL PSYC, V39, P817 Stahmer A. C., 1999, CHILD LANG TEACH THE, V15, P29, DOI 10.1191/026565999672332808 Striano T, 1999, BRIT J DEV PSYCHOL, V17, P551, DOI 10.1348/026151099165474 Whalen C, 2003, J CHILD PSYCHOL PSYC, V44, P456, DOI 10.1111/1469-7610.00135 NR 41 TC 57 Z9 59 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2006 VL 36 IS 5 BP 655 EP 664 DI 10.1007/s10803-006-0108-z PG 10 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900009 PM 16810564 ER PT J AU O'Riordan, M Passetti, F AF O'Riordan, Michelle Passetti, Filippo TI Discrimination in autism within different sensory modalities SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; discrimination; auditory; tactile ID PERVASIVE DEVELOPMENTAL DISORDERS; EARLY INFANTILE-AUTISM; VISUAL-SEARCH; ENHANCED DISCRIMINATION; FOLLOW-UP; CHILDREN; LANGUAGE; ABNORMALITIES; MODULATION; STIMULI AB Recent studies have suggested that unusual visual processing in autism might stem from enhanced visual discrimination. Although there are also many anecdotal reports of auditory and tactile processing disturbances in autism these have received comparatively little attention. It is possible that the enhanced discrimination ability in vision in autism might extend to other modalities and further that they may underlie many reports of unusual touch and audition. The present study investigated the performance of children with and without autism on auditory and tactile discrimination tasks and revealed superior auditory but comparable tactile discrimination in autism relative to controls. These results extend previous findings of perceptual discrimination in autism and may be relevant for a neuro-developmental hypothesis of the disorder. C1 Autism Res Ctr, Dept Dev Psychiat, Cambridge CB2 3AH, England. Univ Cambridge, Cambridge, England. RP O'Riordan, M (reprint author), Autism Res Ctr, Dept Dev Psychiat, Douglas House,18b Trumpington Rd, Cambridge CB2 3AH, England. 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PD JUL PY 2006 VL 36 IS 5 BP 665 EP 675 DI 10.1007/s10803-006-0106-1 PG 11 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900010 PM 16639532 ER PT J AU de Jonge, MV Kemner, C van Engeland, H AF de Jonge, Maretha V. Kemner, Chantal van Engeland, Herman TI Superior disembedding performance of high-functioning individuals with autism spectrum disorders and their parents: The need for subtle measures SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; broader phenotype; Embedded Figures Test; parents; pervasive developmental disorder; weak central coherence ID DIAGNOSTIC OBSERVATION SCHEDULE; WEAK CENTRAL COHERENCE; ASPERGER-SYNDROME; ENHANCED DISCRIMINATION; COGNITIVE PHENOTYPE; INFANTILE-AUTISM; VISUAL-SEARCH; CHILDREN; MIND; PERCEPTION AB We assessed the disembedding performance on the Embedded Figures Test (EFT) of high-functioning subjects with autism or autism spectrum disorders from multi-incidence families and the performance of their parents. The individuals with autism spectrum disorders were significantly faster than matched controls in locating the shape, but their parents were not faster than a control group of parents. However, both the individuals with autism spectrum disorders and their fathers made significantly fewer incorrect attempts before finding the right shape than matched controls. These results suggest that the number of incorrect attempts is a more subtle measure than accuracy or response time for assessing superior disembedding skills and therefore may be useful in the assessment of individuals with autism spectrum disorders. C1 Univ Utrecht, Dept Child & Adolescent Psychiat, NL-3508 GA Utrecht, Netherlands. Maastricht Univ, Maastricht, Netherlands. RP de Jonge, MV (reprint author), Univ Utrecht, Dept Child & Adolescent Psychiat, HP B01-201,POB 85500, NL-3508 GA Utrecht, Netherlands. EM M.V.Jonae@umcutrecht.nl CR Achenbach T. 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C., 1997, MANUAL YOUTH SELF RE Verhulst F. C., 1997, MANUAL TEACHERS REPO Verhulst FC, 1996, MANUAL CHILD BEHAV C, P4 Witkin HA, 1971, MANUAL EMBEDDED FIGU NR 42 TC 32 Z9 32 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2006 VL 36 IS 5 BP 677 EP 683 DI 10.1007/s10803-006-0113-2 PG 7 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900011 PM 16612576 ER PT J AU Benson, PR AF Benson, Paul R. TI The impact of child symptom severity on depressed mood among parents of children with ASD: The mediating role of stress proliferation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE stress proliferation; autism; ASD; parent depression; social support; symptom severity ID SOCIAL SUPPORT; DEVELOPMENTAL-DISABILITIES; EARLY INTERVENTION; AUTISTIC-CHILDREN; LIFE STRESS; SELF-REPORT; MOTHERS; FATHERS; ADJUSTMENT; FAMILY AB Stress proliferation (the tendency of stressors to engender additional stressors in other life domains) is explored in a sample of 68 parents of children identified with ASD. Regression analyses showed that parent depression was predicted by both child symptom severity and by stress proliferation and that stress proliferation partially mediated the effect of child symptom severity on parent depression. 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TI Hyperserotoninemia and altered immunity in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE autism; hyperserotoninemia; immune response; serotonin ID DELAYED-TYPE HYPERSENSITIVITY; PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN TRANSPORTER 5-HTT; KILLER-CELL CYTOTOXICITY; WHOLE-BLOOD SEROTONIN; T-LYMPHOCYTE FUNCTION; PLATELET SEROTONIN; 1ST-DEGREE RELATIVES; TRANSMISSION DISEQUILIBRIUM; 5-HYDROXYINDOLEACETIC ACID AB One of the most consistent biological findings in autism is elevated whole blood serotonin (5-HT) levels found in about 1/3 of cases. Immune abnormalities are also commonly observed in this disorder. Given 5-HT's role as an immunomodulator, possible connections between 5-HT and immune abnormalities in autism are explored in this review. Areas of focus include hyperserotoninemia and cellular immune function, autoantibodies to 5-HT receptors, and 5-HT's role in autoimmunity. Further research is needed to determine the interactions between neuropsychiatric and immune dysfunction in autism and related disorders. C1 Univ Utah, Dept Neurol, Salt Lake City, UT 84132 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT 84132 USA. RP Fujinami, RS (reprint author), Univ Utah, Dept Neurol, 30 N 1900 E,3R330 SOM, Salt Lake City, UT 84132 USA. 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Autism Dev. Disord. PD JUL PY 2006 VL 36 IS 5 BP 697 EP 704 DI 10.1007/s10803-006-0100-7 PG 8 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900013 PM 16614791 ER PT J AU Papanikolaou, K Paliokosta, E Gyftodimou, J Kolaitis, G Vgenopoulou, S Sarri, C Tsiantis, J AF Papanikolaou, Katerina Paliokosta, Elena Gyftodimou, Jolanda Kolaitis, Gerassimos Vgenopoulou, Sofia Sarri, Catherine Tsiantis, John TI A case of partial trisomy of chromosome 8p associated with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; genetics; chromosome 8; partial trisomy 8p ID MILD MENTAL-RETARDATION; SHORT ARM; DYSMORPHIC FEATURES; TANDEM DUPLICATION; GENOMIC SCREEN; 8P23.1; REGION; DISORDERS; LINKAGE; GENE AB We report on a case of a 6-year-old female with partial trisomy 8p(21-23) associated with autism, mild dysmorphic features, and moderate learning disability. Although mental retardation is a common finding in patients with mosaic trisomy 8 or partial trisomy of various regions of chromosome 8, only two cases associated with autism have been reported so far. Also, in our case clinical manifestations were mild compared to other patients with duplication of the same region of chromosome 8. Although there has been no strong evidence for linkage on chromosome 8 in any of the genome-wide linkage studies so far, the possibility that this segment includes genes involved in the etiology of autism should be further explored. C1 Univ Athens, Dept Child Psychiat, Agia Sophia Childrens Hosp, Athens 11527, Greece. Agia Sophia Childrens Hosp, Inst Child Hlth, Dept Genet, Athens 11527, Greece. RP Papanikolaou, K (reprint author), Univ Athens, Dept Child Psychiat, Agia Sophia Childrens Hosp, Athens 11527, Greece. 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Autism Dev. Disord. PD JUL PY 2006 VL 36 IS 5 BP 705 EP 709 DI 10.1007/s10803-006-0104-3 PG 5 WC Psychology, Developmental SC Psychology GA 075ZX UT WOS:000239927900014 PM 16602035 ER PT J AU Korkmaz, B Benbir, G Demirbilek, V AF Korkmaz, Baris Benbir, Gulcin Demirbilek, Veysi TI Migration abnormality in the left cingulate gyrus presenting with autistic disorder SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID CHILDHOOD AUTISM; GLUCOSE-METABOLISM; SPECTRUM DISORDER; INFANTILE-AUTISM; BLOOD-FLOW; BRAIN; CORTEX; NEUROANATOMY AB Autism, characterized by an impairment in communication, including language, narrowly focused interests, and poor sociability, is a neurodevelopmental disorder of still largely unknown pathogenesis. In children with autistic symptomatology, the most consistent functional or anatomic abnormalities are found in the cingulate gyrus, particularly in the anterior regions. Neuronal migration malformations caused by incomplete neuronal migration and characterized by loss of the normal gyral patterns in the cerebral hemispheres and prominent disorganization of the cerebral cortical cytoarchitecture are generally associated with profound neurologic deficits, epilepsy, and autism. In this report, we present a case with an isolated migration abnormality located in the anterior part of the left cingulate gyrus who was admitted with the complaints of epileptic seizures and autism. In addition, the role of the localization of the migration abnormality in the Autism is a neurodevelopmental disorder characterized by an impairment in communication, including language, a lack of imagination, poor sociability, narrowly focused interests, and stereotypies.(1) Although the pathogenesis of the disorder is still largely unknown, various pathologic abnormalities have been shown in many different areas of the brain, including the cerebellum, limbic system, and brain stem,(2) as well as changes in brain weight,(3) increased brain size,(4-6) minicolunmar pathology in various parts of the cerebral cortex,(7) changes in white- and gray-matter volume,(8,9) and aberrations in brain metabolism and blood flow(10) in different parts of the brain. Increased cell impact, decreased neuron size, and aberrant dendritic branching are reported in different structures of the limbic system.(11) In children with autistic symptomatology, the most consistent functional or anatomic abnormalities are found in the cingulate gyrus, particularly in the anterior regions. 10 Many of the above-mentioned pathologic abnormalities in autism might have started at an earlier stage of neural development, possibly before the third gestational month 3 at a time when neuronal migration prevails. Indeed, neuronal migration problems, not an infrequent cause of intractable epilepsy and mental retardation, have also been reported in autistic cases(2,3). C1 Univ Istanbul, Div Child Neurol, Dept Neurol, Cerrahpasa Fac Med, TR-34303 Cerrahpasa, Turkey. RP Korkmaz, B (reprint author), Univ Istanbul, Div Child Neurol, Dept Neurol, Cerrahpasa Fac Med, TR-34303 Cerrahpasa, Turkey. 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Child Neurol. PD JUL PY 2006 VL 21 IS 7 BP 600 EP 604 DI 10.2310/7010.2006.00141 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 075SR UT WOS:000239906000011 PM 16970852 ER PT J AU Tanguay, PE AF Tanguay, Peter E. TI The neurobiology of autism, 2nd edition SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Book Review C1 Univ Louisville, Sch Med, Louisville, KY 40292 USA. RP Tanguay, PE (reprint author), Univ Louisville, Sch Med, Louisville, KY 40292 USA. CR Bauman M. L., 2005, NEUROBIOLOGY AUTISM NR 1 TC 0 Z9 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JUL PY 2006 VL 67 IS 7 BP 1161 EP 1162 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 070TU UT WOS:000239548300027 ER PT J AU Badcock, C Crespi, B AF Badcock, C. Crespi, B. TI Imbalanced genomic imprinting in brain development: an evolutionary basis for the aetiology of autism SO JOURNAL OF EVOLUTIONARY BIOLOGY LA English DT Review DE autism; evolution; genomic imprinting; social behaviour ID PRADER-WILLI-SYNDROME; PARENT-OF-ORIGIN; GLUTAMIC-ACID DECARBOXYLASE; HIGH-FUNCTIONING AUTISM; RECEPTOR SUBUNIT GENES; RECIPROCAL SOCIAL-BEHAVIOR; FAMILY-BASED ASSOCIATION; GAMMA-AMINOBUTYRIC-ACID; GROWTH-FACTOR-II; RETT-SYNDROME AB We describe a new hypothesis for the development of autism, that it is driven by imbalances in brain development involving enhanced effects of paternally expressed imprinted genes, deficits of effects from maternally expressed genes, or both. This hypothesis is supported by: (1) the strong genomic-imprinting component to the genetic and developmental mechanisms of autism, Angelman syndrome, Rett syndrome and Turner syndrome; (2) the core behavioural features of autism, such as self-focused behaviour, altered social interactions and language, and enhanced spatial and mechanistic cognition and abilities, and (3) the degree to which relevant brain functions and structures are altered in autism and related disorders. The imprinted brain theory of autism has important implications for understanding the genetic, epigenetic, neurological and cognitive bases of autism, as ultimately due to imbalances in the outcomes of intragenomic conflict between effects of maternally vs. paternally expressed genes. C1 London Sch Econ, Dept Sociol, London, England. Simon Fraser Univ, Behav Ecol Res Grp, Burnaby, BC V5A 1S6, Canada. RP Crespi, B (reprint author), Simon Fraser Univ, Dept Biol Sci, Burnaby, BC V5A 1S6, Canada. 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Growth modelling analyses were used to explore: (1) whether mothers of children with Down syndrome demonstrated distinct patterns of stress during their children's early development, compared with mothers of children with other developmental disabilities; and (2) whether there was a relation between child behavioural characteristics and the level and rate of change in stress observed in each population. Method The stress trajectories of mothers of young children with Down syndrome (n = 25) and a mixed-aetiology comparison group (n = 49) were estimated, using growth modelling on data collected at ages of 15, 30 and 45 months. Results On average, stress in the mixed comparison group was higher at Time 1 and remained unchanged over time, while stress in the Down syndrome group was lower at Time 1 but increased steadily. 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Method We compared the non-verbal IQ of adolescents and young adults with co-morbid FXS and autism (n = 10) with those with only FXS (n = 44). We then created a subsample of those with FXS only, matched on non-verbal IQ, mental age and gender (n = 21) to the subsample of those with co-morbid FXS and autism. We compared the two groups on measures of expressive language, receptive language (lexical, grammatical morphology and syntactic patterns), and a theory of mind task. Results Those with co-morbid FXS and autism had lower non-verbal IQs than those with only FXS. The participants with co-morbid FXS and autism did not perform as well as the cognitive ability- and gender-matched participants with only FXS on the three measures of receptive language or the theory of mind task; there were no differences on the expressive language measure. Conclusions Our findings support the notion that those with co-morbid FXS and autism represent a distinct subtype of FXS, with more impairment in receptive language and theory of mind even when controlling for their lower non-verbal IQ relative to those with only FXS. The greater cognitive impairments observed in those with co-morbid FXS and autism continues into adolescence and young adulthood; and the autism seen in those with FXS appears to be the same as idiopathic autism. C1 Univ Wisconsin, Waisman Ctr 157, Madison, WI 53705 USA. Kennedy Krieger Inst, Baltimore, MD USA. Johns Hopkins Univ, Baltimore, MD USA. RP Lewis, P (reprint author), Univ Wisconsin, Waisman Ctr 157, 1500 Highland Ave, Madison, WI 53705 USA. 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PD JUL PY 2006 VL 50 BP 532 EP 545 DI 10.1111/j.1365-2788.2006.00803.x PN 7 PG 14 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 048ED UT WOS:000237929500006 PM 16774638 ER PT J AU Ashwood, P Wills, S Van De Water, J AF Ashwood, Paul Wills, Sharifia Van De Water, Judy TI The immune response in autism: a new frontier for autism research SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Review DE autism spectrum disorder (ASD); neurodevelopment; neurokine; immunity; inflammation; cytokines ID DISEASE VIRUS-INFECTION; CENTRAL-NERVOUS-SYSTEM; OBSESSIVE-COMPULSIVE DISORDER; LYMPHOCYTE CYTOKINE PROFILES; SEROTONIN TRANSPORTER GENE; SPECTRUM DISORDERS; TOURETTES-SYNDROME; CEREBROSPINAL-FLUID; GASTROINTESTINAL SYMPTOMS; SCHIZOPHRENIC-PATIENTS AB Autism spectrum disorders (ASD) are part of a broad spectrum of neurodevelopmental disorders known as pervasive developmental disorders, which occur in childhood. They are characterized by impairments in social interaction, verbal and nonverbal communication and the presence of restricted and repetitive stereotyped behaviors. At the present time, the etiology of ASD is largely unknown, but genetic, environmental, immunological, and neurological factors are thought to play a role in the development of ASD. Recently, increasing research has focused on the connections between the immune system and the nervous system, including its possible role in the development of ASD. These neuroimmune interactions begin early during embryogenesis and persist throughout an individual's lifetime, with successful neurodevelopment contingent upon a normal balanced immune response. Immune aberrations consistent with a dysregulated immune response, which so far, have been reported in autistic children, include abnormal or skewed T helper cell type I (T(H)1)/T(H)2 cytokine profiles, decreased lymphocyte numbers, decreased T cell mitogen response, and the imbalance of serum immunoglobulin levels. In addition, autism has been linked with autoimmunity and an association with immune-based genes including human leukocyte antigen (HLA)-DRB1 and complement C4 alleles described. There is potential that such aberrant immune activity during vulnerable anti critical periods of neurodevelopment could participate in the generation of neurological dysfunction characteristic of ASD. This review will examine the status of the research linking the immune response with ASD. C1 Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Sacramento, CA 95817 USA. 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Leukoc. Biol. PD JUL PY 2006 VL 80 IS 1 BP 1 EP 15 DI 10.1189/jlb.1205707 PG 15 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA 119MD UT WOS:000243015500001 PM 16698940 ER PT J AU Bhuiyan, ZA Klein, M Hammond, P van Haeringen, A Mannens, MMAM Van Berckelaer-Onnes, I Hennekam, RCM AF Bhuiyan, ZA Klein, M Hammond, P van Haeringen, A Mannens, MMAM Van Berckelaer-Onnes, I Hennekam, RCM TI Genotype-phenotype correlations of 39 patients with Cornelia De Lange syndrome: the Dutch experience SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID BRACHMANN-DELANGE SYNDROME; DEVELOPMENTAL BEHAVIOR CHECKLIST; SISTER-CHROMATID COHESION; NIPPED-B; MENTAL-RETARDATION; FACIAL MORPHOLOGY; NIPBL MUTATIONS; INDIVIDUALS; HOMOLOG; VARIABILITY AB Background: Cornelia de Lange syndrome ( CdLS) is a multiple congenital anomaly syndrome characterised by a distinctive facial appearance, prenatal and postnatal growth deficiency, psychomotor delay, behavioural problems, and malformations of the upper extremities. Recently mutations in NIPBL, the human homologue of the Drosophila Nipped-B gene, were found to cause CdLS. Mutations have been found in 39% of reported cases. Methods: Patients were enrolled in the study and classified into one of four groups based on clinical examination: classic, mild, possible, or definitively not CdLS. Three dimensional photography was taken of 20 subjects, and compared between groups. Behaviour was assessed with specific attention to autism. We searched for mutations in NIPBL and correlated genotype with phenotype. Results : We found mutations in 56% of cases. Conclusions: Truncating mutations were generally found to cause a more severe phenotype but this correlation was not absolute. Three dimensional facial imaging demonstrated the potential for classifying facial features. Behavioural problems were highly correlated with the level of adaptive functioning, and also included autism. No correlation of behaviour with the type of mutation was found. C1 UCL, Inst Child Hlth, Clin & Mol Genet Unit, London WC1N 1EH, England. Acad Med Ctr, Dept Paediat, Amsterdam, Netherlands. Univ Amsterdam, Dept Clin Genet, Acad Med Ctr, Amsterdam, Netherlands. Leiden Univ, Dept Clin Child & Adolescent Studies, Fac Social & Behav Sci, Leiden, Netherlands. UCL, Eastman Dent Inst, London, England. UMCL, Dept Clin Genet, Leiden, Netherlands. RP Hennekam, RCM (reprint author), UCL, Inst Child Hlth, Clin & Mol Genet Unit, 30 Guilford St, London WC1N 1EH, England. 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PD JUL PY 2006 VL 98 SU 1 BP 27 EP 27 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 066QQ UT WOS:000239245600063 ER PT J AU Chauhan, A Chauhan, V Cohen, IL Mehta, P Brown, WT Barshatzky, M AF Chauhan, A. Chauhan, V Cohen, I. L. Mehta, P. Brown, W. T. Barshatzky, M. TI Increased oxidative stress and inflammation in autism SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract CT 7th Biennial Meeting of the Asian-Pacific-Society-for-Neurochemistry CY JUL 02-05, 2006 CL Singapore, SINGAPORE SP Asia Pacific Soc Neurochem C1 NYS Inst Basic Res Dev Disabil, New York, NY USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JUL PY 2006 VL 98 SU 1 BP 29 EP 29 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 066QQ UT WOS:000239245600071 ER PT J AU Atkin, K Lorch, MP AF Atkin, Keith Lorch, Marjorie Perlman TI Hyperlexia in a 4-year-old boy with Autistic Spectrum Disorder SO JOURNAL OF NEUROLINGUISTICS LA English DT Article DE hyperlexia; autism; reading acquisition; reading comprehension ID WORD RECOGNITION; READING-SKILLS; LANGUAGE DISORDER; YOUNG-CHILDREN; COMPREHENSION; ANNOTATION; AWARENESS; ABILITY AB This paper presents a case study of a 4-year-old boy with Autistic Spectrum Disorder and a mental age of approximately 1:5 who demonstrates precocious oral-reading behaviour in the absence of spontaneous speech. Tests of reading regular and irregular words, pseudowords, homographic heterophones, single sentences and texts were carried out. 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Neurolinguist. PD JUL PY 2006 VL 19 IS 4 BP 253 EP 269 DI 10.1016/J.jneuroling.2005.11.006 PG 17 WC Linguistics; Neurosciences; Psychology, Experimental SC Linguistics; Neurosciences & Neurology; Psychology GA 082NN UT WOS:000240393700001 ER PT J AU Love, R AF Love, R TI A mouse model of autism? SO LANCET NEUROLOGY LA English DT News Item ID SOCIAL-INTERACTION; PTEN CR Greer JM, 2006, NEURON, V50, P343, DOI 10.1016/j.neuron.2006.04.021 Kwon CH, 2006, NEURON, V50, P377, DOI 10.1016/j.neuron.2006.03.023 NR 2 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1474-4422 J9 LANCET NEUROL JI Lancet Neurol. PD JUL PY 2006 VL 5 IS 7 BP 559 EP 559 DI 10.1016/S1474-4422(06)70486-0 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 058PE UT WOS:000238676100009 ER PT J AU Seeman, CC AF Seeman, Corey TI The only boy in the world: On having a son with autism. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Michigan, Kresge Business Adm Lib, Ann Arbor, MI 48109 USA. RP Seeman, CC (reprint author), Univ Michigan, Kresge Business Adm Lib, Ann Arbor, MI 48109 USA. CR BLASTLAND M, 2006, ONLY BOY WORLD HAVIN NR 1 TC 0 Z9 0 PU REED BUSINESS INFORMATION PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD JUL PY 2006 VL 131 IS 12 BP 96 EP 96 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 062IG UT WOS:000238937200244 ER PT J AU Parr, JR Lamb, JA Bailey, AJ Monaco, AP AF Parr, JR Lamb, JA Bailey, AJ Monaco, AP TI Response to paper by Molloy et al.: Linkage on 21q and 7q in autism subset with regression SO MOLECULAR PSYCHIATRY LA English DT Letter ID HUMAN GENOME; SCREEN; MAP C1 Univ Oxford, IMGSAC, Sect Child & Adolescent Psychiat, Oxford OX3 7JX, England. RP Parr, JR (reprint author), Univ Oxford, IMGSAC, Sect Child & Adolescent Psychiat, Oxford OX3 7JX, England. EM jeremyparr@doctors.org.uk RI Monaco, Anthony/A-4495-2010; Bailey, Anthony/J-2860-2014 OI Monaco, Anthony/0000-0001-7480-3197; Bailey, Anthony/0000-0003-4257-972X CR Abecasis GR, 2002, NAT GENET, V30, P97, DOI 10.1038/ng786 Bailey A, 1998, HUM MOL GENET, V7, P571 Palferman S, 2001, AM J HUM GENET, V69, P570 Kong A, 2002, NAT GENET, V31, P241, DOI 10.1038/ng917 Kong X, 2004, AM J HUM GENET, V75, P1143, DOI 10.1086/426405 Kruglyak L, 1996, AM J HUM GENET, V58, P1347 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Molloy CA, 2005, MOL PSYCHIATR, V10, P741, DOI 10.1038/sj.mp.4001691 NR 9 TC 6 Z9 6 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD JUL PY 2006 VL 11 IS 7 BP 617 EP 619 DI 10.1038/sj.mp.4001833 PG 4 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 057IW UT WOS:000238590500002 PM 16801976 ER PT J AU Molloy, CA Keddache, M Martin, L AF Molloy, CA Keddache, M Martin, L TI Response to paper by Molloy et al.: Linkage on 21q and 7q in autism subset with regression - Response by Dr Molloy SO MOLECULAR PSYCHIATRY LA English DT Letter C1 Cincinnati Childrens Hosp Med Ctr, Ctr Biostat & Epidemiol, Div Dev & Behav Pediat, Cincinnati, OH USA. Cincinnati Childrens Hosp Med Ctr, Div Human Genet, Cincinnati, OH USA. RP Molloy, CA (reprint author), Cincinnati Childrens Hosp Med Ctr, Ctr Biostat & Epidemiol, Div Dev & Behav Pediat, Cincinnati, OH USA. EM Cynthia.molloy@cchmc.org NR 0 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD JUL PY 2006 VL 11 IS 7 BP 619 EP 619 DI 10.1038/sj.mp.4001829 PG 1 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 057IW UT WOS:000238590500003 ER PT J AU Glazebrook, CM Elliott, D Lyons, J AF Glazebrook, Cheryl M. Elliott, Digby Lyons, James TI A kinematic analysis of how young adults with and without autism plan and control goal-directed movements SO MOTOR CONTROL LA English DT Article DE autism spectrum disorder; movement control; motor; manual aiming ID SPECTRUM DISORDER; DOWN-SYNDROME; CHILDREN; ACCURACY; TASK AB We examined the planning and control of goal-directed aiming movements in young adults with autism. Participants performed rapid manual aiming movements to one of two targets. We manipulated the difficulty of the planning and control process by varying both target size and amplitude of the movements. Consistent with previous research, participants with autism took longer to prepare and execute movements, particularly when the index of difficulty was high. Although there were no group differences for accuracy, participants with autism exhibited more temporal and spatial variability over the initial phase of the movement even though mean peak accelerations and velocities were lower than for control participants. Our results suggest that although persons with autism have difficulty specifying muscular force, they compensate for this initial variability during limb deceleration. Perhaps persons with autism have learned to keep initial impulses low to minimize the spatial variability that needs to be corrected for during the online control phase of the movement. C1 McMaster Univ, Dept Kinesiol, Hamilton, ON L8S 4K1, Canada. RP Glazebrook, CM (reprint author), McMaster Univ, Dept Kinesiol, Hamilton, ON L8S 4K1, Canada. 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Ma, Deqiong Whitehead, Patrice L. Martin, Eden R. Wright, Harry H. Abramson, Ruth K. Hussman, John P. Haines, Jonathan L. Cuccaro, Michael L. Gilbert, John R. Pericak-Vance, Margaret A. TI Investigation of autism and GABA receptor subunit genes in multiple ethnic groups SO NEUROGENETICS LA English DT Article DE autism; SNPs; GABA receptors; association; ethnicity ID LINKAGE DISEQUILIBRIUM; ASSOCIATION; DISORDER; PREVALENCE; PEDIGREES; SEROTONIN; FAMILIES; GENETICS; EPILEPSY; TESTS AB Autism is a neurodevelopmental disorder of complex genetics, characterized by impairment in social interaction and communication, as well as repetitive behavior. Multiple lines of evidence, including alterations in levels of GABA and GABA receptors in autistic patients, indicate that the GABAergic system, which is responsible for synaptic inhibition in the adult brain, may be involved in autism. Previous studies in our lab indicated association of noncoding single nucleotide polymorphisms (SNPs) within a GABA receptor subunit gene on chromosome 4, GABRA4, and interaction between SNPs in GABRA4 and GABRB1 (also on chromosome 4), within Caucasian autism patients. Studies of genetic variation in African-American autism families are rare. Analysis of 557 Caucasian and an independent population of 54 African-American families with 35 SNPs within GABRB1 and GABRA4 strengthened the evidence for involvement of GABRA4 in autism risk in Caucasians (rs17599165, p=0.0015; rs1912960, p=0.0073; and rs17599416, p=0.0040) and gave evidence of significant association in African-Americans (rs2280073, p=0.0287 and rs16859788, p=0.0253). The GABRA4 and GABRB1 interaction was also confirmed in the Caucasian dataset (most significant pair, rs1912960 and rs2351299; p=0.004). Analysis of the subset of families with a positive history of seizure activity in at least one autism patient revealed no association to GABRA4; however, three SNPs within GABRB1 showed significant allelic association; rs2351299 (p=0.0163), rs4482737 (p=0.0339), and rs3832300 (p=0.0253). These results confirmed our earlier findings, indicating GABRA4 and GABRB1 as genes contributing to autism susceptibility, extending the effect to multiple ethnic groups and suggesting seizures as a stratifying phenotype. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27706 USA. Univ S Carolina, Sch Med, Columbia, SC USA. Hussman Fdn, Ellicott City, MD USA. Vanderbilt Univ, Ctr Med, Ctr Human Genet Res, Nashville, TN USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27706 USA. 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Piven, Joseph Hazlett, Heather Cody Smith, Rachel Gimpel Ho, Sean Gee, James C. Gerig, Guido TI User-guided 3D active contour segmentation of anatomical structures: Significantly improved efficiency and reliability SO NEUROIMAGE LA English DT Article DE computational anatomy; image segmentation; caudate nucleus; 3D active contour models; open source software; validation; anatomical objects ID QUANTITATIVE VOLUMETRIC-ANALYSIS; IMAGE SEGMENTATION; MR-IMAGES; BRAIN; CAUDATE; MODEL; VISUALIZATION; SCHIZOPHRENIA; MORPHOMETRY; VALIDATION AB Active contour segmentation and its robust implementation using level set methods are well-established theoretical approaches that have been studied thoroughly in the image analysis literature. Despite the existence of these powerful segmentation methods, the needs of clinical research continue to be fulfilled, to a large extent, using slice-by-slice manual tracing. To bridge the gap between methodological advances and clinical routine, we developed an open source application called ITK-SNAP, which is intended to make level set segmentation easily accessible to a wide range of users, including those with little or no mathematical expertise. This paper describes the methods and software engineering philosophy behind this new tool and provides the results of validation experiments performed in the context of an ongoing child autism neuroimaging study. The validation establishes SNAP intrarater and interrater reliability and overlap error statistics for the caudate nucleus and finds that SNAP is a highly reliable and efficient alternative to manual tracing. Analogous results for lateral ventricle segmentation are provided. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Penn, Dept Radiol, Penn Image Comp & Sci Lab, Philadelphia, PA 19104 USA. Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. 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It is an integral function of the primary care medical home and an appropriate responsibility of all pediatric health care professionals. This statement provides an algorithm as a strategy to support health care professionals in developing a pattern and practice for addressing developmental concerns in children from birth through 3 years of age. The authors recommend that developmental surveillance be incorporated at every well-child preventive care visit. Any concerns raised during surveillance should be promptly addressed with standardized developmental screening tests. In addition, screening tests should be administered regularly at the 9-, 18-, and 30-month visits. (Because the 30-month visit is not yet a part of the preventive care system and is often not reimbursable by third-party payers at this time, developmental screening can be performed at 24 months of age. In addition, because the frequency of regular pediatric visits decreases after 24 months of age, a pediatrician who expects that his or her patients will have difficulty attending a 30-month visit should conduct screening during the 24-month visit.) The early identification of developmental problems should lead to further developmental and medical evaluation, diagnosis, and treatment, including early developmental intervention. Children diagnosed with developmental disorders should be identified as children with special health care needs, and chronic-condition management should be initiated. Identification of a developmental disorder and its underlying etiology may also drive a range of treatment planning, from medical treatment of the child to family planning for his or her parents. 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D, 1976, INTERVENTION STRATEG WERNER EE, 1968, CHILD DEV, V39, P1063, DOI 10.1111/j.1467-8624.1968.tb04485.x Zwaigenbaum L, 2005, INT J DEV NEUROSCI, V23, P143, DOI 10.1016/j.ijdevneu.2004.05.001 NR 45 TC 330 Z9 331 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUL PY 2006 VL 118 IS 1 BP 405 EP 420 DI 10.1542/peds.2006-1231 PG 16 WC Pediatrics SC Pediatrics GA 059II UT WOS:000238726100049 ER PT J AU Fombonne, E Zakarian, R Bennett, A Meng, LY McLean-Heywood, D AF Fombonne, E Zakarian, R Bennett, A Meng, LY McLean-Heywood, D TI Pervasive developmental disorders in Montreal, Quebec, Canada: Prevalence and links with immunizations SO PEDIATRICS LA English DT Article DE school-aged child; autism; Asperger syndrome; childhood disintegrative disorder; pervasive developmental disorder; prevalence; epidemiology; immunization; thimerosal; ethylmercury; measles vaccine; MMR ID THIMEROSAL-CONTAINING VACCINES; AUTISTIC SPECTRUM DISORDER; RUBELLA VACCINATION; CAUSAL ASSOCIATION; UNITED-KINGDOM; PRESCHOOL-CHILDREN; POPULATION; MEASLES; MUMPS; MMR AB BACKGROUND. The prevalence of pervasive developmental disorders has increased in recent years. Links with the measles component of the measles-mumps-rubella vaccine and the cumulative exposure to thimerosal through other vaccines have been postulated. OBJECTIVES. The purpose of this work was to estimate the pervasive developmental disorder prevalence in Montreal, Canada, in cohorts born from 1987 to 1998 and evaluate the relationship of trends in pervasive developmental disorder rates with: (1) changes in cumulative exposure to ethylmercury (thimerosal) occurring through modifications in the immunization schedule of young children and (2) trends in measles-mumps-rubella vaccination use rates and the introduction of a 2-measles-mumps-rubella dosing schedule during the study period. METHODS. We surveyed 27 749 children born from 1987 to 1998 attending 55 schools from the largest Anglophone school board. Children with pervasive developmental disorders were identified by a special needs team. The cumulative exposure by age 2 years to thimerosal was calculated for 1987-1998 birth cohorts. Ethylmercury exposure ranged from medium (100-125 mu g) from 1987 to 1991 to high (200-225 mu g) from 1992 to 1995 to nil from 1996 onwards when thimerosal was entirely discontinued. Measles-mumps-rubella coverage for each birth cohort was estimated through surveys of vaccination rates. The immunization schedule included a measles-mumps-rubella single dose at 12 months of age up to 1995, and a second measles-mumps-rubella dose at 18 months of age was added on after 1996. RESULTS. We found 180 children (82.8% males) with a pervasive developmental disorder diagnosis who attended the surveyed schools, yielding a prevalence for pervasive developmental disorder of 64.9 per 10 000. The prevalence for specific pervasive developmental disorder subtypes were, for autistic disorder: 21.6 of 10 000; for pervasive developmental disorder not otherwise specified: 32.8 of 10 000; and for Asperger syndrome: 10.1 of 10 000. A statistically significant linear increase in pervasive developmental disorder prevalence was noted during the study period. The prevalence of pervasive developmental disorder in thimerosal-free birth cohorts was significantly higher than that in thimerosal-exposed cohorts (82.7 of 10 000 vs 59.5 of 10 000). Using logistic regression models of the prevalence data, we found no significant effect of thimerosal exposure used either as a continuous or a categorical variable. Thus, thimerosal exposure was unrelated to the increasing trend in pervasive developmental disorder prevalence. These results were robust when additional analyses were performed to address possible limitations because of the ecological nature of the data and to evaluate potential effects of misclassification on exposure or diagnosis. Measles-mumps-rubella vaccination coverage averaged 93% during the study interval with a statistically significant decreasing trend from 96.1% in the older birth cohorts (1988-89) to similar to 92.4% in younger birth cohorts (1996-1998). Thus, pervasive developmental disorder rates significantly increased when measles-mumps-rubella vaccination uptake rates significantly decreased. In addition, pervasive developmental disorder prevalence increased at the same rate before and after the introduction in 1996 of the second measles-mumps-rubella dose, suggesting no increased risk of pervasive developmental disorder associated with a 2-measles-mumps-rubella dosing schedule before age 2 years. Results held true when additional analyses were performed to test for the potential effects of misclassification on exposure or diagnostic status. Thus, no relationship was found between pervasive developmental disorder rates and 1- or 2-dose measles-mumps-rubella immunization schedule. CONCLUSIONS. The prevalence of pervasive developmental disorder in Montreal was high, increasing in recent birth cohorts as found in most countries. Factors accounting for the increase include a broadening of diagnostic concepts and criteria, increased awareness and, therefore, better identification of children with pervasive developmental disorders in communities and epidemiologic surveys, and improved access to services. The findings ruled out an association between pervasive developmental disorder and either high levels of ethylmercury exposure comparable with those experienced in the United States in the 1990s or 1- or 2-dose measles-mumps-rubella vaccinations. 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Rev. PD JUL PY 2006 VL 113 IS 3 BP 483 EP 525 DI 10.1037/0033-295X.113.3.483 PG 43 WC Psychology; Psychology, Multidisciplinary SC Psychology GA 059UJ UT WOS:000238757400003 PM 16802879 ER PT J AU Schreck, KA Williams, K AF Schreck, Kimberly A. Williams, Keith TI Food preferences and factors influencing food selectivity for children with autism spectrum disorders SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE food; children; autism spectrum disorder AB Although clinicians and parents widely accept that children with autism spectrum disorder exhibit more feeding problems than their typically developing peers, little information is available concerning the characteristic food items accepted by these children or the possible factors contributing to these feeding problems. This article used an informant-based questionnaire to survey parents of children with autism spectrum disorders (N= 138) to determine: (a) the types of feeding problems their children typically exhibit, (b) the food items their children prefer, (c) the relationship of feeding problems to family eating preferences, and (d) the relationship of the diagnostic characteristics of autism to feeding behavior. Results indicated that the children preferred fewer types of food items within groups than their families; however, family food preferences appeared to influence food selection more than the diagnostic characteristics of autism. (c) 2005 Elsevier Ltd. All rights reserved. C1 Penn State Univ, Psychol Program, Middletown, PA 17047 USA. Hershey Med Ctr, Hershey, PA USA. RP Schreck, KA (reprint author), Penn State Univ, Psychol Program, 777 W Harrisburg Pike,W157 Olmsted Bldg, Middletown, PA 17047 USA. 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TI Stepping Stones Triple P: A pilot study to evaluate acceptability of the program by parents of a child diagnosed with an Autism Spectrum Disorder SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE Stepping Stones Triple P; Autism Spectrum Disorder; parenting programs ID FOLLOW-UP; BEHAVIOR; PREVALENCE AB The experience of parents of children with Autism Spectrum Disorder (ASD) in standard parenting programs has not been researched, although anecdotal evidence suggests that they do not find them acceptable. Forty-two parents of children with ASD were asked to view a DVD explaining individual parenting strategies from Stepping Stones, a new branch of the Triple P program targeted specifically at parents of children with disabilities. Parents were asked to rate each strategy for acceptability, usability and behavioural intention, i.e., their intention to use the strategy. Additionally, parental attributions and parental perceived control were explored as possible barriers to positive evaluations of Stepping Stones parenting strategies. A focus group of parents was used to gather more detailed parent response to the program. Parent responses to the program were generally positive and attribution of the child's behaviour to uncontrollable factors was found to predict higher ratings of usability. The results were interpreted within the context of Weiner's attributional theory and the theory of reasoned action. The limitations of this study and suggestions for future research are discussed. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Sofronoff, K (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. 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PD JUL-AUG PY 2006 VL 27 IS 4 BP 364 EP 380 DI 10.1016/j.ridd.2005.05.003 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 072OD UT WOS:000239681800002 PM 16051461 ER PT J AU Fossett, B Mirenda, P AF Fossett, Brenda Mirenda, Pat TI Sight word reading in children with developmental disabilities: A comparison of paired associate and picture-to-text matching instruction SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE literacy; sight word recognition; paired associate learning; matching ID VOCABULARY; ACQUISITION; PROMPTS; PROGRAM; AUTISM AB Numerous instructional techniques have been used to teach sight word reading skills to individuals with developmental disabilities. The results of research incorporating paired associate instruction, in which familiar pictures are paired with unknown print stimuli, suggest that pictures "block" (i.e., interfere with) learners' ability to recognize novel text. On the other hand, there is some evidence that both stimulus fading and picture-to-text matching techniques can be used successfully to teach sight word recognition. The present study used an adapted alternating treatments design [Sindelar, R T., Rosenberg, M. S., & Wilson, R. J. (1985). An adapted alternating treatments design for instructional research. Education and Treatment of Children, 8, 67-76] to compare paired associate and picture-to-text matching techniques for teaching a small corpus of unknown words to two children with developmental disabilities. Results indicated that the picture-to-text matching condition was more effective than the paired associate condition for developing a small sight word vocabulary. Follow-up data for one participant showed that skills developed using the picture-to-text matching strategy were maintained 4 months after intervention. 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McPherson, K. TI Snoezelen multi-sensory environments: Task engagement and generalization SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE snoezelen multi-sensory environments; autism; challenging behaviors; intellectual disability; occupational therapy ID MENTAL-RETARDATION; CHILDREN; ADULTS; ROOM AB These experiments explored whether behavioral improvements observed during Snoezelen OT treatment sessions carried over to two different settings for three people with moderate/severe intellectual disability, autism and severe challenging behaviors. Experiment I explored engagement during a functional task immediately following the treatment sessions while experiment 2 explored changes in the frequencies of challenging behaviors on the days after treatment sessions. lnvestigators found carryover for two of the three participants to both post-session engagement as well as to the daily frequency of challenging behaviors on days following the OT sessions. (c) 2005 Elsevier Ltd. All rights reserved. C1 Lifespire, Woodhaven, NY 11421 USA. Downstate Med Ctr, Brooklyn, NY USA. RP Kaplan, H (reprint author), Lifespire, 84-03 96th St, Woodhaven, NY 11421 USA. EM howiedr@aol.com CR Ashby M., 1995, BRIT J OCCUPATIONAL, V58, P303 Ayres J., 1972, SENSORY INTEGRATION CARR E, 2000, COMMUNICATION BASED Cook T. D., 1979, QUASIEXPERIMENTATION Cuvo AJ, 2001, RES DEV DISABIL, V22, P183, DOI 10.1016/S0891-4222(01)00067-1 Dunn W, 1997, INFANT YOUNG CHILD, V9, P23 Houghton S, 1998, J INTELLECT DEV DIS, V23, P267, DOI 10.1080/13668259800033761 Kazdin A. E., 1982, SINGLE CASE RES DESI Pfeiffer Beth, 2003, Occup Ther Int, V10, P175, DOI 10.1002/oti.184 RIESMAN JE, 1992, SENSORY INTEGRATION Shapiro M, 1997, BRIT J DEV DISABIL, V43, P140 SHROUT PE, 1979, PSYCHOL BULL, V86, P420, DOI 10.1037//0033-2909.86.2.420 Singh NN, 2004, RES DEV DISABIL, V25, P285, DOI 10.1016/j.ridd.2003.08.003 NR 13 TC 11 Z9 11 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD JUL-AUG PY 2006 VL 27 IS 4 BP 443 EP 455 DI 10.1016/j.ridd.2005.05.007 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 072OD UT WOS:000239681800007 PM 16122905 ER PT J AU Holden, B Gitlesen, JP AF Holden, Borge Gitlesen, Jens Petter TI A total population study of challenging behaviour in the county of Hedmark, Norway: Prevalence, and risk markers SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE challenging behaviour; mental retardation; prevalence; risk markers ID SELF-INJURIOUS-BEHAVIOR; PSYCHIATRIC-SYMPTOMS; MENTAL-RETARDATION; PEOPLE; ADULTS; DISABILITIES; HANDICAP AB Studies in Britain and the US indicate that 10-15% of people with mental retardation show challenging behaviour, like attacking others (aggression), self-injurious behaviour, destruction, and other difficult, disruptive or socially unacceptable acts. Most researchers indicate that challenging behaviour is more common among adolescents and young adults, among males, is associated with autism, and increases with lack of communication skills and severity of mental retardation. These factors can be understood as risk markers, and some of them can be decreased by preventive and treatment interventions, at least in principle. The present study confirmed most of the previous findings, with some exceptions: the prevalence of more demanding challenging behaviour was somewhat lower in the present study, and no association between gender and challenging behaviour was found. We also concluded that declining prevalence of challenging behaviour at older ages is not a result of a young age structure of the population. (c) 2005 Elsevier Ltd. All rights reserved. C1 Habiliteringstjenesten Voksne, N-2312 Ottestad, Norway. Stavanger Univ Coll, Stavanger, Norway. 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Dev. Disabil. PD JUL-AUG PY 2006 VL 27 IS 4 BP 456 EP 465 DI 10.1016/j.ridd.2005.06.001 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 072OD UT WOS:000239681800008 PM 16137857 ER PT J AU Maldonado, GG Velasquez, VMJ AF Maldonado, Gerardo Garcia Joffre Velasquez, Victor Manuel TI Psychopharmacotherapy in children and adolescents general principles. A review SO SALUD MENTAL LA English DT Article DE psychopharmacotherapy; children and adolescents; general principles; child psychiatry ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; OBSESSIVE-COMPULSIVE DISORDER; MEDICATION ALGORITHM PROJECT; RANDOMIZED CONTROLLED-TRIAL; CONSENSUS CONFERENCE PANEL; MANIC-DEPRESSIVE ILLNESS; PLACEBO-CONTROLLED TRIAL; DEFICIT HYPERACTIVITY DISORDER; AGGRESSIVE YOUTH TRAAY; ANXIETY DISORDERS AB The work of Charles Bradley done in 1937, which reports the effects of Benzedrine in 30 pediatric patients that had behaviour problems, is a classic document considered by many as the beginning of child psychopharmacotherapy. In spite of a coordinated effort made by the National Institute of Mental Health in the United States carried out by a panel, called "Conferences on Infantile Research in Psychopharmacology", for many years this practice kept being inarticulate. Psychopharmacotherapy in adults with psychiatric diseases has had a different development. During the decade of 1950 substances such as chlorpromazine and tricycle antidepressives started to be used in clinical practice and between 1980 and 1990 new products were developed for treating schizophrenia, depression and mania. Even if there is no such as the "ideal drug", the new psychopharmacological developments have allowed patients to have a better quality of life. In pediatric population the difficulty to conduct controlled clinical tests has been a constant; for this reason the practice of child psychopharmacotherapy keeps facing challenges; also, in the United States several very strict norms have been dictated in order to endorse the security and efficacy of a product for infantile use. Other problems faced today in clinical practice are the excesive use of medications for minors prescribed by people without enough practice and academic information, and also the deficient therapeutic results provoked by wrong prescriptions. But the worst of all are the false promises made to relatives and patients, on the usage of products or substances that have not been tested by a rigorous scientific scrutiny, specially concerning diffused clinical problems such as the Attention Deficit Hyperactivity Disorder (ADHD) or Autism. These facts, most of all, determine the rejection and fear for medications and become an adverse variable that we must face continuously. The main objective of this work is to make a review about the general principles that are suggested for a good psychopharmacotherapy on children and teen-alters, a practice that must always be part of a planned multimode treatment that follows an adequate paidopsychiatric evaluation. A right diagnose will always be important for the appropriate selection of the medication. The development of taxonomies such as those described in the Mental Disorders Statistics and Diagnostic Manual of the American Psychiatric Association or by the International Classification of Diseases of the World Health Organization, have allowed the existence of an order in the elaboration of paidopsychiatric diagnosis, that even if being mainly descriptive, allow to make a more structured clinical work. The parameters for the psychiatric evaluation of children and teenagers recommended by the American Academy of Child and Adolescent Psychiatry (AACAP) in 1997 is an example of the importance that proves the attention on minors, its objective is to give a guide without pretending to make it a golden standard. The selection of a medication must be based on two premises: a diagnose of the disorder itself, and on the other hand, the recognition of target symptoms. Considering this interrelation will allow a more acceptable evaluation on the risks and benefits of a pharmacological prescription for children and teen-alters. Thus pediatric psychopharmacotherapy must be based on the correlation between the actions and effects of drugs and the biochemical and evolving aspects of the disorder, but it will also be necessary that the professional be aware of the changes that inevitably will take place in the dynamic of absorption, distribution and elimination of the medications according to the stage of the biological child's development. When someone deals with very small children, it is almost impossible for the child psychiatrist to get direct information as it is for children to understand the information that the expert would pretend to give them. This constrains to consider the cognitive and verbal realities proper of each stage of the development, so the direct evaluation of the small patient must be complemented with reports of a multi-informers system. It will be fundamental to consider also that small children have little differentiated emotions and that it must not be ignored that for them concepts such as time and space are difficult to understand. Clinical exploration through recreational activities will be a primordial tool in the daily work with children. It will also be recommendable that the plan of the treatment be organized jointly with the parents of the minor in order to inform them completely about the goals and objectives of the prescription of a drug; the participation of the small patient must be included too. It must not be forgotten that the pharmacological treatment is part of a more integral attention program in which other experts must participate, such as pedagogues, clinical psychologists or language therapists, a fact that will be more common than irregular. The therapeutic adherence is a variable that must be constantly checked. If it is carried out irregularly or the wrong dose of the recommended drug is taken, the presence of symptoms as a result of the abrupt interruption of the medication could be confused with the adverse collateral effects, which would make worse the clinical condition. Pediatric patients must have a complete medical history complemented by a physical and neurological evaluation, which must be included in the registry of vital constants as well as size and weight of the minor; other registers could be more convenient if they are considered to be needed. The support on laboratory surveys plays an important roll and at the present time the recommendation for making an electrocardiography evaluation previous to the administration of some drugs is more accepted; in this sense it is undoubtedly important to consider the recommendations proposed by the American Association of Cardiology for monitoring the cardiovascular function of children and teen-agers who receive medications after prolonged periods of time. Polypharmacy is a common practice; due to this fact, the interaction between drug/ drug must be carefully valued. The child psychiatric evaluation must be made with the support of structured or semi-structured interviews for the clinical diagnosis and with evaluation scales for measuring the severity of the specific symptoms or global clinical conditions. The strategy for choosing a plan of pharmacological treatment for the pediatric patient must be made individually; in this sense, the development of algorithms for the administration of medications on children and teen-agers has been the result of many efforts in order to make prescriptions more rational and neat. The revision of controlled clinical tests on the efficacy and security of these agents in the pediatric population is fundamental for the election of a prescription. The responsibility of the professional that prescribes a medication devolves on structuring a plan of formal treatment and an individualized monitoring according to the stages of the treatment (beginning, maintenance and interruption). As it is expected, the expert must reach the maximum therapeutic benefit in a child or an adolescent with the minimum of collateral effects, evaluating always the risk and the benefits. Some authors recommend the prescription of drugs on children and teen-agers only for short periods of time as the non-desirable effects in long terms are not quite well known. There are no specific times for stopping the administration of a drug. However, it is recommended that during the stages of the treatment, clinical changes in minors be watched and registered rigorously, in order to be able to reduce or stop the dose in the appropriate moment, even in cases of clinical conditions such as schizophrenia, depression or development generalized disorders. The main objective of this clinical work will be that the quality of life of the minor becomes optimum. C1 Hosp Psiquiatrico Tampico, Unidad Invest, Tampico 89130, Tamaulipas, Mexico. Hosp Psiquiatrico Tampico, Clin Ninos & Adolescentes, Tampico 89130, Tamaulipas, Mexico. RP Maldonado, GG (reprint author), Hosp Psiquiatrico Tampico, Unidad Invest, Ejercito Mexicano 1403,Col Allende, Tampico 89130, Tamaulipas, Mexico. 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Neurosci. PD JUN 28 PY 2006 VL 26 IS 26 BP 6897 EP 6906 DI 10.1523/JNEUROSCI.1712-06.2006 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 060LT UT WOS:000238804400002 PM 16807320 ER PT J AU Donnay, A AF Donnay, A TI Origins of autism SO NEW SCIENTIST LA English DT Letter NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD JUN 17 PY 2006 VL 190 IS 2556 BP 26 EP 26 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 056KF UT WOS:000238520900030 ER PT J AU Powers, MK AF Powers, MK TI Improving visual skills: a new internet application SO JOURNAL OF MODERN OPTICS LA English DT Article; Proceedings Paper CT Biennial Conference on Development in Vision Enhancement Technology and Their Evaluation CY JUN 03-04, 2005 CL Morgantown, WV SP Natl Sci Fdn, USA Res Off, Natl Aeronaut & Space Adm, West Virginia Univ Eye Inst HO West Virginia Univ ID PERFORMANCE AB The object of this paper is to describe an internet-based system and technique for improving performance on visuomotor tasks. The technique can be used in any setting where the internet can be accessed, and can be adapted for improving a variety of visual tasks. Sample learning curves for acquiring the visual skills of accommodative facility, saccadic tracking and binocular fusion are presented, from three subjects ages 7 and 9, including one child diagnosed with autism. The database structure of the system allows powerful data storage and retrieval options for use in providing feedback on performance, online monitoring of progress by an external observer, and statistical analysis of group and individual data. C1 Gemstone Fdn, Inst Res, Rodeo, CA 94572 USA. RP Powers, MK (reprint author), Gemstone Fdn, Inst Res, 575 San Pablo Ave,Suite D, Rodeo, CA 94572 USA. 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Opt. PD JUN 15 PY 2006 VL 53 IS 9 BP 1313 EP 1323 DI 10.1080/09500340600619148 PG 11 WC Optics SC Optics GA 048IA UT WOS:000237939600012 ER PT J AU Gundelfinger, R AF Gundelfinger, Ronnie TI Early identification of children at risk for Autism Spectrum Disorder SO SWISS MEDICAL WEEKLY LA English DT Meeting Abstract C1 Univ Zurich, Dept Child & Adolescent Psychiat, CH-8006 Zurich, Switzerland. NR 0 TC 0 Z9 0 PU E M H SWISS MEDICAL PUBLISHERS LTD PI MUTTENZ PA FARNSBURGERSTR 8, CH-4132 MUTTENZ, SWITZERLAND SN 1424-7860 J9 SWISS MED WKLY JI Swiss Med. Wkly. PD JUN 10 PY 2006 VL 136 SU 151 BP 9S EP 9S PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 052IO UT WOS:000238227600019 ER PT J AU Locher, A Weber, P AF Locher, A. Weber, P. TI Neurobiological findings in children with infantile autism SO SWISS MEDICAL WEEKLY LA English DT Meeting Abstract C1 Univ Childrens HOsp Basel, Basel, Switzerland. NR 0 TC 0 Z9 0 PU E M H SWISS MEDICAL PUBLISHERS LTD PI MUTTENZ PA FARNSBURGERSTR 8, CH-4132 MUTTENZ, SWITZERLAND SN 1424-7860 J9 SWISS MED WKLY JI Swiss Med. Wkly. PD JUN 10 PY 2006 VL 136 SU 151 BP 31S EP 31S PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 052IO UT WOS:000238227600093 ER PT J AU Lancefield, K Nosarti, C Rifkin, L Allin, M Sham, P Murray, R AF Lancefield, Kristin Nosarti, Chiara Rifkin, Larry Allin, Matt Sham, Pak Murray, Robin TI Cerebral asymmetry in 14 year olds born very preterm SO BRAIN RESEARCH LA English DT Article DE adolescent; fronto-occipital; structural asymmetry; torque ID ULTRASOUND APPEARANCE; HUMAN-BRAIN; SCHIZOPHRENIA; INFANTS; ADOLESCENTS; VOLUMES; MRI; HANDEDNESS; RELATIVES; BIRTH AB The normal pattern of cerebral asymmetry maybe altered in neuro developmental disorders such as autism and schizophrenia. Babies born very preterm have an increased risk of brain damage, and brain abnormalities which persist into adolescence. This study aimed to ascertain whether preterm. birth affects the development of fronto-occipital asymmetry. Structural MRI (magnetic resonance imaging) scans from 14 year old individuals born very preterm. (n = 61; mean age 14 years 11 months; 29 male) and age-matched full-term controls (n = 49; mean age 14 years 11 months; 31 male) under-went morphometric analysis, using well-validated stereological methods. Measurements of right and left prefrontal, premotor, sensorimotor and occipitoparietal regional volumes were made and asymmetry indices calculated. These factors underwent a reductive factor analysis. There were no significant between-group differences in fronto-occipital asymmetry between the preterm. adolescents and their full-term counterparts. It seems unlikely, therefore, that preterm birth per se deviates the development of normal fronto-occipital asymmetry. 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PD JUN 6 PY 2006 VL 1093 BP 33 EP 40 DI 10.1016/j.brainres.2006.03.097 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 064CZ UT WOS:000239068100005 PM 16696955 ER PT J AU [Anonymous] AF [Anonymous] TI Sensory perceptual issues in autism and Asperger syndrome: Different sensory experiences-different perceptual worlds. SO ADOLESCENCE LA English DT Book Review CR Bogdashina O, 2003, SENSORY PERCEPTUAL I NR 1 TC 0 Z9 0 PU LIBRA PUBLISHERS INC PI SAN DIEGO PA 3089C CLAIREMONT DR SUITE 383, SAN DIEGO, CA 92117 USA SN 0001-8449 J9 ADOLESCENCE JI Adolescence PD SUM PY 2006 VL 41 IS 162 BP 393 EP 393 PG 1 WC Psychology, Developmental SC Psychology GA 079IN UT WOS:000240169400015 ER PT J AU [Anonymous] AF [Anonymous] TI Engaging autism: Using the floortime approach to help children relate, communicate, and think. SO ADOLESCENCE LA English DT Book Review CR Greenspan SI, 2006, ENGAGING AUTISM USIN NR 1 TC 0 Z9 0 PU LIBRA PUBLISHERS INC PI SAN DIEGO PA 3089C CLAIREMONT DR SUITE 383, SAN DIEGO, CA 92117 USA SN 0001-8449 J9 ADOLESCENCE JI Adolescence PD SUM PY 2006 VL 41 IS 162 BP 399 EP 399 PG 1 WC Psychology, Developmental SC Psychology GA 079IN UT WOS:000240169400025 ER PT J AU Giarelli, E Pinto-Martin, J AF Giarelli, E. Pinto-Martin, J. TI Feasibility of obtaining parental consent for special education record review in autism surveillance. SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Meeting Abstract CT 2nd North American Congress of Epidemiology CY JUN 21-24, 2006 CL Seattle, WA C1 Univ Penn, Ctr Autism & Dev Disabil Res Epidemiol, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 1 PY 2006 VL 163 IS 11 SU S BP S12 EP S12 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 051AP UT WOS:000238132900046 ER PT J AU Hertz-Picciotto, I AF Hertz-Picciotto, I. TI Is the incidence of autism rising? And do we have an epidemic? SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Meeting Abstract CT 2nd North American Congress of Epidemiology CY JUN 21-24, 2006 CL Seattle, WA C1 Univ Calif Davis, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 1 PY 2006 VL 163 IS 11 SU S BP S86 EP S86 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 051AP UT WOS:000238132900344 ER PT J AU Kancherla, V Dennis, LK AF Kancherla, V. Dennis, L. K. TI A meta-analysis of prenatal, perinatal, and neonatal risks for autism. SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Meeting Abstract CT 2nd North American Congress of Epidemiology CY JUN 21-24, 2006 CL Seattle, WA C1 Univ Iowa, Iowa City, IA 52242 USA. NR 0 TC 0 Z9 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 1 PY 2006 VL 163 IS 11 SU S BP S20 EP S20 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 051AP UT WOS:000238132900081 ER PT J AU Nicholas, JS King, L Carpenter, L Jenner, W Charles, J AF Nicholas, J. S. King, L. Carpenter, L. Jenner, W. Charles, J. TI Characteristics of children with autism spectrum disorders in South Carolina. SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Meeting Abstract CT 2nd North American Congress of Epidemiology CY JUN 21-24, 2006 CL Seattle, WA C1 Med Univ S Carolina, Dept Biostat Bioinformat & Epidemiol, Columbia, SC USA. NR 0 TC 0 Z9 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 1 PY 2006 VL 163 IS 11 SU S BP S20 EP S20 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 051AP UT WOS:000238132900079 ER PT J AU Descheemaeker, MJ Govers, V Vermeulen, P Fryns, JP AF Descheemaeker, MJ Govers, V Vermeulen, P Fryns, JP TI Pervasive developmental disorders in Prader-Willi syndrome: The Leuven experience in 59 subjects and controls SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE pervasive developmental disorders (PDD); Prader-Willi syndrome (PWS); mental retardation; behavioral phenotype; autism; learning disabilities; uniparental maternal disomy (UPD); chromosome 15 ID MATERNAL UNIPARENTAL DISOMY; ADAPTIVE-BEHAVIOR SCALES; MALADAPTIVE BEHAVIOR; MENTAL-RETARDATION; PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; PSYCHIATRIC-DISORDERS; COMPULSIVE BEHAVIOR; CHILDREN; AUTISM AB In the present study we investigated the co-morbidity of pervasive developmental disorder (PDD) in 59 Prader-Willi syndrome (PWS) individuals and in 59 non-specific mentally retarded controls, matched for IQ, gender, and age. The 'Pervasive Developmental Disorder Mentally Retardation Scale' (PDD-MRScale), a screening questionnaire based on the DSM-III-R criteria for PDD, has been applied in the PWS group and in the control group. Results of the present study revealed a striking autistic-like behavioral phenotype in the majority of the PWS individuals, particularly deficits in the quality of language and communication and of imagination and interests. This intersection with autistic symptomatology is an important addition to the behavioral phenotype in PWS persons. A first approach to delineate subtypes of autistic symptomalogy among PWS persons was performed. Nineteen percent of the PWS group did meet the full diagnostic DSM-III-R criteria for PDD in comparison with 15% in the control group. Results revealed that a higher IQ in PWS does not protect to develop genuine PDD and that uniparental disomy/imprinting mutation as genetic origin seems to be an additional risk factor for developing genuine PDD. The results of the present study suggest the importance of reconsidering the commonly recognized obsessive-compulsive like behavior in PWS persons within the broader spectrum of autism disorders. (c) 2006 Wiley-Liss, Inc. C1 Univ Leuven, Ctr Human Genet, B-3000 Louvain, Belgium. Ctr Concrete Commun, Ghent, Belgium. RP Descheemaeker, MJ (reprint author), Univ Leuven, Ctr Human Genet, Herestr 49, B-3000 Louvain, Belgium. 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J. Med. Genet. A PD JUN 1 PY 2006 VL 140A IS 11 BP 1136 EP 1142 DI 10.1002/ajmg.a.31235 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 049BK UT WOS:000237990300002 PM 16646032 ER PT J AU Leonard, H De Klerk, N Bourke, J Bower, C AF Leonard, H De Klerk, N Bourke, J Bower, C TI Maternal health in pregnancy and intellectual disability in the offspring: A population-based study SO ANNALS OF EPIDEMIOLOGY LA English DT Article DE maternal health; pregnancy; intellectual disability; mental retardation; asthma; diabetes; Australia ID URINARY-TRACT-INFECTIONS; FETAL VALPROATE SYNDROME; AGE-CHILDREN BORN; WESTERN-AUSTRALIA; MENTAL-RETARDATION; DIABETIC MOTHERS; RISK-FACTORS; SCHOOL-AGE; NEWBORN ENCEPHALOPATHY; PERINATAL RISK AB PURPOSE: The aim of the study is to investigate the relationship between common maternal conditions and intellectual disability (ID) of unknown cause in the offspring. METHODS: Information about the maternal health of children with and without ID was obtained by using record linkage. For mothers with specific medical conditions, proportions of children with mild to moderate ID, severe ID, and autism spectrum disorder (ASD) with ID were compared with those who did not have ID. RESULTS: There was an increased risk for mild to moderate ID in children of mothers with asthma (odds ratio [OR], 1.52; confidence interval [CI], 1.26-1.831), diabetes (OR, 1.69; CI, 1.26-2.27), a renal or urinary condition (OR, 2.09; CI, 1.39-3.14), and epilepsy (OR, 3.53; CI, 2.56-4.84). ASD risk was increased for children of women with diabetes (OR, 2.89; CI, 1.28-6.51) and epilepsy (OR, 4.5 7; CI, 1.69-12.3 1). For anemia (n = 1101), there was an increased risk for severe ID (OR, 5.26; CI, 2.16-12.80). CONCLUSIONS: The increased risk for ID in offspring of mothers with such conditions as asthma and diabetes is particularly important for disadvantaged or ethnic populations, for whom these conditions are more prevalent and may be less well managed. C1 Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, Perth, WA 6872, Australia. RP Leonard, H (reprint author), Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, POB 855, Perth, WA 6872, Australia. 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Epidemiol. PD JUN PY 2006 VL 16 IS 6 BP 448 EP 454 DI 10.1016/j.annepidem.2005.05.002 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 049ZS UT WOS:000238057500006 PM 16182562 ER PT J AU ElChaar, GM Maisch, NM Augusto, LMG Wehring, HJ AF ElChaar, GM Maisch, NM Augusto, LMG Wehring, HJ TI Efficacy and safety of naltrexone use in pediatric patients with autistic disorder SO ANNALS OF PHARMACOTHERAPY LA English DT Article DE autism; autistic disorder; naltrexone; pediatrics ID PLACEBO-CONTROLLED CROSSOVER; BETA-ENDORPHIN LEVELS; DOUBLE-BLIND; INFANTILE-AUTISM; DEVELOPMENTAL DISORDERS; SELF-INJURY; CHILDREN; PREVALENCE; WITHDRAWAL; SYMPTOMS AB OBJECTIVE: To review the efficacy and safety of naltrexone in pediatric patients with autistic disorder (AD). DATA SOURCES: Using the terms pediatric, child, naltrexone, autism, and autistic disorder, a literature search was performed using MEDLINE (1966-May 18, 2006) and the International Pharmaceutical Abstracts (1971-May 18, 2006) database. The references of these articles were scanned for additional relevant literature. STUDY SELECTION AND DATA EXTRACTION: All articles describing or evaluating the efficacy and/or safety of naltrexone in pediatric patients with AD were included in this review. Three case reports, 8 case series, and 14 clinical studies were identified as pertinent. DATA SYNTHESIS: Naltrexone has been used most commonly at doses ranging from 0.5 to 2 mg/kg/day and found to be predominantly effective in decreasing self-injurious behavior. Naltrexone may also attenuate hyperactivity, agitation, irritability, temper tantrums, social withdrawal, and stereotyped behaviors. Patients may also exhibit improved attention and eye contact. Transient sedation was the most commonly reported adverse event. Small sample size, short duration, and inconsistent evaluative methods characterize the available research. CONCLUSIONS: A child affected by AD may benefit from a trial of naltrexone therapy, particularly if the child exhibits self-injurious behavior and other attempted therapies have failed. Serious adverse effects have not been reported in short-term studies. C1 St Johns Univ, Coll Pharm, Clin Pharm Practice Dept, Queens, NY 11439 USA. St Johns Univ, Coll Pharm & Allied Hlth Profess, Queens, NY 11439 USA. Long Isl Jewish Med Ctr, Dept Pharm, Drug Informat Serv, New Hyde Pk, NY 11040 USA. Zucker Hillside Hosp, N Shore Long Isl Jewish Hlth Syst, Glen Oaks, NY USA. RP Augusto, LMG (reprint author), St Johns Univ, Coll Pharm, Clin Pharm Practice Dept, SAH Rm 114,8000 Utopia Pkwy, Queens, NY 11439 USA. 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Pharmacother. PD JUN PY 2006 VL 40 IS 6 BP 1086 EP 1095 DI 10.1345/aph.1G499 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 054IF UT WOS:000238369300011 PM 16735648 ER PT J AU Munson, J Dawson, G Abbott, R Faja, S Webb, SJ Friedman, SD Shaw, D Artru, A Dager, SR AF Munson, Jeffrey Dawson, Geraldine Abbott, Robert Faja, Susan Webb, Sara Jane Friedman, Seth D. Shaw, Dennis Artru, Alan Dager, Stephen R. TI Amygdalar volume and behavioral development in autism SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID FACIAL EXPRESSIONS; INFANTILE-AUTISM; TEMPORAL-LOBE; BRAIN; CHILDREN; SPECTRUM; NEUROANATOMY; RECOGNITION; ADOLESCENTS; HIPPOCAMPUS AB Context: The amygdala is associated with socioemotional function and has been implicated in the pathophysiology of autism. Objective: To examine the relationship between amygdalar volume at ages 3 and 4 years and severity of clinical course and outcome at 6 years of age in children with autism spectrum disorder. Design: Magnetic resonance images acquired at 3 and 4 years of age were used to measure total cerebral, amygdalar, and hippocampal volumes. Acquisition of social and communication skills was assessed semiannually using the Vineland Adaptive Behavior Scales. Hierarchical linear models were used to predict variability in individual linear growth trajectories as a function of IQ, total cerebral, and amygdalar or hippocampal volumes. Setting: Longitudinal study of children with autism spectrum disorder. Participants: Forty-five children with autism spectrum disorders between 3 and 6 years of age. Main Outcome Measure: Linear growth trajectory of age equivalence Vineland communication and social scores. Results: Larger right amygdalar volume was associated with more severe social and communication impairments at ages 3 and 4 years. Larger right amygdalar volume also was predictive of poorer social and communication abilities at age 6 years, even after controlling for IQ and total cerebral volume. Parallel analyses with hippocampal volumes found no relationship to social or communication development. Conclusions: Larger right amygdalar volume at 3 and 4 years of age, but not left amygdalar, hippocampal, or total cerebral volume, is associated with a more severe clinical course and worse outcome at age 6 years in children with autism spectrum disorder. These results provide additional evidence that amygdalar development is implicated in the behavioral impairments found in autism. C1 Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98105 USA. Univ Washington, Autism Ctr, Seattle, WA 98105 USA. Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98105 USA. Univ Washington, Dept Psychol, Seattle, WA 98105 USA. Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98105 USA. Univ Washington, Dept Educ Psychol, Seattle, WA 98105 USA. Univ Washington, Dept Anesthesiol, Seattle, WA 98105 USA. Univ Washington, Dept Bioengn, Seattle, WA 98105 USA. Childrens Hosp, Seattle, WA USA. Reg Med Ctr, Seattle, WA USA. RP Dager, SR (reprint author), Univ Washington, Sch Med, Dept Radiol, 1100 NE 45th St,Suite 555, Seattle, WA 98105 USA. 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Gen. Psychiatry PD JUN PY 2006 VL 63 IS 6 BP 686 EP 693 DI 10.1001/archpsyc.63.6.686 PG 8 WC Psychiatry SC Psychiatry GA 049XD UT WOS:000238050200011 PM 16754842 ER PT J AU Lord, C Risi, S DiLavore, PS Shulman, C Thurm, A Pickles, A AF Lord, C Risi, S DiLavore, PS Shulman, C Thurm, A Pickles, A TI Autism from 2 to 9 years of age SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID DIAGNOSTIC OBSERVATION SCHEDULE; PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIORAL TREATMENT; SPECTRUM DISORDERS; SOCIAL-BEHAVIOR; FIELD TRIAL; FOLLOW-UP; DSM-IV; CHILDREN; ABNORMALITIES AB Context: Autism represents an unusual pattern of development beginning in the infant and toddler years. Objectives: To examine the stability of autism spectrum diagnoses made at ages 2 through 9 years and identify features that predicted later diagnosis. Design: Prospective study of diagnostic classifications from standardized instruments including a parent interview (Autism Diagnostic Interview-Revised [ADI-R]), an observational scale (Pre-Linguistic Autism Diagnostic Observation Schedule/Autism Diagnostic Observation Schedule [ADOS]), and independent clinical diagnoses made at ages 2 and 9 years compared with a clinical research team's criterion standard diagnoses. Setting: Three inception cohorts: consecutive referrals for autism assessment to (1) state-funded community autism centers, (2) a private university autism clinic, and (3) case controls with developmental delay from community clinics. Participants: At 2 years of age, 192 autism referrals and 22 developmentally delayed case controls; 172 children seen at 9 years of age. Main Outcome Measures: Consensus best-estimate diagnoses at 9 years of age. Results: Percentage agreement between best-estimate diagnoses at 2 and 9 years of age was 67, with a weighted kappa of 0.72. Diagnostic change was primarily accounted for by movement from pervasive developmental disorder not otherwise specified to autism. Each measure at age 2 years was strongly prognostic for autism at age 9 years, with odds ratios of 6.6 for parent interview, 6.8 for observation, and 12.8 for clinical judgment. Once verbal IQ (P = .001) was taken into account at age 2 years, the ADI-R repetitive domain (P = .02) and the ADOS social (P = .05) and repetitive domains (P = .005) significantly predicted autism at age 9 years. Conclusions: Diagnostic stability at age 9 years was very high for autism at age 2 years and less strong for pervasive developmental disorder not otherwise specified. Judgment of experienced clinicians, trained on standard instruments, consistently added to information available from parent interview and standardized observation. C1 Univ Michigan, Autism & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. Univ N Carolina, Chapel Hill, NC USA. 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Gen. Psychiatry PD JUN PY 2006 VL 63 IS 6 BP 694 EP 701 DI 10.1001/archpsyc.63.6.694 PG 8 WC Psychiatry SC Psychiatry GA 049XD UT WOS:000238050200012 PM 16754843 ER PT J AU Igliori, GC Damasceno, BP AF Igliori, GC Damasceno, BP TI Theory of mind and the frontal lobes SO ARQUIVOS DE NEURO-PSIQUIATRIA LA English DT Article DE theory of mind; frontal lesions; cognition; neuropsychological tests ID MENTAL-STATE; CHILDREN; REPRESENTATION; LANGUAGE; PATIENT; AUTISM; ADULTS AB Background: Theory of mind (ToM) is the ability to attribute mental states to other individuals. Its cerebral organization is not enough established, even though the literature suggests the relevant role of the frontal lobes. Objective: To evaluate frontal lobe patients and controls in ToM tests. Method: We studied 20 patients with lesions limited to the frontal lobes (as shown by CT or MRI), and 10 normal control subjects by means of ToM tests (recognizing himself in mirrors, false belief, first and second order ToM tasks), as well as tests of other cognitive functions (counter-proofs). Results: Patients and controls performed similarly in ToM tests. There was significant difference between frontal subgroups (left, right, bifrontal) in the double-bluff task (second order ToM) (p=0.021), without relation to verbal fluency (p=0.302) or delayed recall ability (p=0.159). The only two patients with deficits in ToM tasks had impairment of social behavior. Conclusion: Frontal lesions do not necessarily implicate in ToM deficits, which may occur when such lesions are associated to disturbance of social behavior. C1 Univ Estadual Campinas, Sch Med, Dept Neurol, BR-13083970 Campinas, SP, Brazil. RP Damasceno, BP (reprint author), Univ Estadual Campinas, Sch Med, Dept Neurol, Box 6111, BR-13083970 Campinas, SP, Brazil. EM damascen@unicamp.br CR Apperly IA, 2004, J COGNITIVE NEUROSCI, V16, P1773, DOI 10.1162/0898929042947928 AVIS J, 1991, CHILD DEV, V62, P460, DOI 10.1111/j.1467-8624.1991.tb01544.x BARONCOHEN S, 1989, BRIT J DEV PSYCHOL, V7, P113 BARONCOHEN S, 1994, BRIT J PSYCHIAT, V165, P640, DOI 10.1192/bjp.165.5.640 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BERTOLUCCI PHF, 1994, ARQ NEURO-PSIQUIAT, V52, P1 CAIXETA L, 2000, THESIS SAO PAULO Caixeta Leonardo, 2002, Psicol. Reflex. Crit., V15, P105, DOI 10.1590/S0102-79722002000100012 Christensen A.L., 1979, LURIAS NEUROPSYCHOLO Dennett D., 1978, BEHAVIOURAL BRAIN SC, V4, P568 Fine C, 2001, BRAIN, V124, P287, DOI 10.1093/brain/124.2.287 FOLSTEIN MF, 1975, J PSYCHIAT RES, V12, P189, DOI 10.1016/0022-3956(75)90026-6 Happe F, 2001, NEUROPSYCHOLOGIA, V39, P83, DOI 10.1016/S0028-3932(00)00093-2 Happe F, 1999, COGNITION, V70, P211, DOI 10.1016/S0010-0277(99)00005-0 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Kaplan E, 1983, BOSTON NAMING TEST KARMILOFFSMITH A, 1995, J COGNITIVE NEUROSCI, V7, P196, DOI 10.1162/jocn.1995.7.2.196 LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 LEZAK MD, 1995, NEUROPSYCHOLOGICAL A PEMER J, 1985, J EXPT CHILD PSYCHOL, V39, P437 POVINELLI DJ, 1995, TRENDS NEUROSCI, V18, P418, DOI 10.1016/0166-2236(95)93939-U PREMACK D, 1978, BEHAV BRAIN SCI, V1, P515 RATCLIFF G, 1979, NEUROPSYCHOLOGIA, V17, P49, DOI 10.1016/0028-3932(79)90021-6 Rey A., 1958, EXAMEN CLIN PSYCHOL *SAS I INC, 1999, SAS STAT AN SYST WIN Saxe R, 2003, NEUROIMAGE, V19, P1835, DOI 10.1016/S1053-8119(03)00230-1 Stone VE, 1998, J COGNITIVE NEUROSCI, V10, P640, DOI 10.1162/089892998562942 Stuss DT, 2001, BRAIN, V124, P279, DOI 10.1093/brain/124.2.279 Tomasello M., 1999, CULTURAL ORIGINS HUM Wechsler D., 1987, WECHSLER MEMORY SCAL WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 NR 32 TC 5 Z9 6 PU ASSOC ARQUIVOS DE NEURO- PSIQUIATRIA PI SAO PAULO SP PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL SN 0004-282X J9 ARQ NEURO-PSIQUIAT JI Arq. Neuro-Psiquiatr. PD JUN PY 2006 VL 64 IS 2A BP 202 EP 206 DI 10.1590/S0004-282X2006000200006 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 050UC UT WOS:000238113200006 PM 16791356 ER PT J AU Elias, AV Assumpcao, FB AF Elias, AV Assumpcao, FB TI Quality of life and autism SO ARQUIVOS DE NEURO-PSIQUIATRIA LA Portuguese DT Article DE quality of life; childhood; autism ID CHILDREN; RELIABILITY; BEHAVIOR; VALIDITY; SCALE AB Objective: To evaluate the index quality of life (QL) in bearers of including upset of the development, Method: 20 autistic childrens, between 4 and 12 years, submitted to the diagnostic evaluation by autistic traces scale-ATA and for the Vineland adaptive behavior scales, needing to obtain in this a quotient of superior development over 70. The data about QL were obtained by the scale of quality of life-AUQEI and compared from the application of Vineland and of AUQEI in a population of normal children, resembling in the sex and in the age. Results: In the evaluation of the ATA, average was 33.75 with 4.95 standard deviation. The indexes of Vineland suggest that normal children have larger probability to present level of appropriated aclaptative behavior than autistic children (p=0.0196). Concerning QL, the general indexes are the same for both groups, indicating positive QL (p=0.744). In the sub domain autonomy, autistic children present higher index (p=0.0048). Conclusion: Autistic childrens present similar indexes of QL than normal childrens. C1 Univ Estadual Campinas, FCM, Dept Psicol Med & Psiquiat, BR-13081970 Campinas, SP, Brazil. Univ Sao Paulo, Fac Med, Dept Psiquiat, Sao Paulo, Brazil. RP Elias, AV (reprint author), Univ Estadual Campinas, FCM, Dept Psicol Med & Psiquiat, Caixa Postal 6111, BR-13081970 Campinas, SP, Brazil. EM atexsandrabender@hotmail.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERS JC, 2004, THESIS RIBEIRAO PRET Assumpcao FB, 1999, ARQ NEURO-PSIQUIAT, V57, P23, DOI 10.1590/S0004-282X1999000100005 Assumpcao FB, 2000, ARQ NEURO-PSIQUIAT, V58, P119, DOI 10.1590/S0004-282X2000000100018 BALLABRIGA MCJ, 1984, REV PSIQUIATR INFANT, V4, P254 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Barreire Simone G, 2003, J Pediatr (Rio J), V79, P55, DOI 10.1590/S0021-75572003000100010 CARTER AC, 1998, J AUTISM DEV DISORD, V28, P55 Klin A, 2000, J CHILD PSYCHOL PSYC, V41, P831, DOI 10.1017/S0021963099006101 Landolt MA, 2002, J PEDIATR-US, V140, P516, DOI 10.1067/mpd.2002.123663 Liss M, 2001, J AUTISM DEV DISORD, V31, P219, DOI 10.1023/A:1010707417274 Magnificat S, 2003, PEDIATR TRANSPLANT, V7, P228 MAGNIFICAT S, 1997, NEUROPSYCHIAT ENFAN, V45, P106 SHEAR J, 2001, INT J PRACTICAL APPR, V25, P40 Sparrow S, 1984, VINELAND ADAPTIVE BE Sprovieri MHS, 2001, ARQ NEURO-PSIQUIAT, V59, P230, DOI 10.1590/S0004-282X2001000200016 SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 VOLKMAR FR, 1991, AM J PSYCHIAT, V148, P1705 *WHOQ GROUP, 1997, MEAS QUAL LIF DEV WO World Health Organization, 2003, INT CLASS FUNCT DIS NR 20 TC 6 Z9 9 PU ASSOC ARQUIVOS DE NEURO- PSIQUIATRIA PI SAO PAULO SP PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL SN 0004-282X J9 ARQ NEURO-PSIQUIAT JI Arq. Neuro-Psiquiatr. PD JUN PY 2006 VL 64 IS 2A BP 295 EP 299 DI 10.1590/S0004-282X2006000200022 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 050UC UT WOS:000238113200022 PM 16791372 ER PT J AU Adams, JB Holloway, CE George, F Quig, D AF Adams, JB Holloway, CE George, F Quig, D TI Analyses of toxic metals and essential minerals in the hair of Arizona children with autism and associated conditions, and their mothers SO BIOLOGICAL TRACE ELEMENT RESEARCH LA English DT Article DE autism; hair analysis; iodine; lithium; potassium ID THYROID-STIMULATING HORMONE; MERCURY; LITHIUM; ELEMENTS; IODINE; WATER AB The objective of this study was to assess the levels of 39 toxic metals and essential minerals in hair samples of children with autism spectrum disorders and their mothers compared to controls. Inductively coupled plasma-mass spectrometry was used to analyze the elemental content of the hair of children with autism spectrum disorders (n=51), a subset of their mothers (n=29), neurotypical children (n=40), and a subset of their mothers (n=25). All participants were recruited from Arizona. Iodine levels were 45% lower in the children with autism (p=0.005). Autistic children with pica had a 38% lower level of chromium (p=0.002). Autistic children with low muscle tone had very low levels of potassium (-66%, p=0.01) and high zinc (31%, p=0.01). The mothers Of Young children with autism had especially low levels of lithium (56% lower, p=0.005), and the young children (ages 3-6 yr) with autism also had low lithium (-30%, p=0.04). Low iodine levels are consistent with previous reports of abnormal thyroid function, which likely affected development of speech and cognitive skills. Low lithium in the mothers likely caused low levels of lithium in the young children, which could have affected their neurological and immunological development. Further investigations of iodine, lithium, and other elements are warranted. C1 Arizona State Univ, Tempe, AZ 85287 USA. Holist Osteopath Med Care, Cave Creek, AZ USA. Doctors Data, St Charles, IL USA. RP Adams, JB (reprint author), Arizona State Univ, Tempe, AZ 85287 USA. 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PD JUN PY 2006 VL 61 IS 1 BP 1 EP 4 DI 10.1016/j.bandc.2006.02.002 PG 4 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600001 PM 16563588 ER PT J AU Blakemore, SJ Tavassoli, T Calo, S Thomas, RM Catmur, C Frith, U Haggard, P AF Blakemore, Sarah-Jayne Tavassoli, Teresa Calo, Susana Thomas, Richard M. Catmur, Caroline Frith, Uta Haggard, Patrick TI Tactile sensitivity in Asperger syndrome SO BRAIN AND COGNITION LA English DT Article DE perception; sensory; somatosensory; autism; tickling; self; other; methods of limits; hypersensitivity; weak central coherence ID WEAK CENTRAL COHERENCE; AUTISM; CHILDREN; PERCEPTION; DEFENSIVENESS; STIMULI AB People with autism and Asperger syndrome are anecdotally said to be hypersensitive to touch. In two experiments, we measured tactile thresholds and suprathreshold tactile sensitivity in a group of adults with Asperger syndrome. In the first experiment, tactile perceptual thresholds were measured. Two frequencies of vibrotactile stimulation were used: 30 and 200Hz. The results demonstrated significantly lower tactile perceptual thresholds in the Asperger group at 200 Hz but not at 30 Hz, thus confirming tactile hypersensitivity but only for one class of stimulus. A second experiment investigated whether self-produced movement affected the perception of touch in a group of adults with Asperger syndrome. A suprathreshold tactile stimulus was produced either by the participant (self-produced condition) or by the experimenter (externally produced condition) and participants were asked to rate the perception of the tactile stimulation. The results demonstrated that, while both Asperger and control groups rated self-produced touch as less tickly than external touch, the Asperger group rated both types of tactile stimulus as significantly more tickly and intense than did the control group. This experiment confirms the finding of tactile hypersensitivity, but shows that the perceptual consequences of self-produced touch are attenuated in the normal way in people with Asperger syndrome. An abnormality in this process cannot therefore account for their tactile hypersensitivity. (c) 2006 Elsevier Inc. All rights reserved. C1 UCL, Dept Psychol, Inst Cognit Neurosci, London WC1N 3AR, England. RP Blakemore, SJ (reprint author), UCL, Dept Psychol, Inst Cognit Neurosci, 17 Queen Sq, London WC1N 3AR, England. 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PD JUN PY 2006 VL 61 IS 1 BP 14 EP 24 DI 10.1016/j.bandc.2005.12.006 PG 11 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600003 PM 16455173 ER PT J AU Happe, F Booth, R Charlton, R Hughes, C AF Happe, Francesca Booth, Rhonda Charlton, Rebecca Hughes, Claire TI Executive function deficits in autism spectrum disorders and attention-deficit/hyperactivity disorder: Examining profiles across domains and ages SO BRAIN AND COGNITION LA English DT Article DE Asperger syndrome; attention-deficit/hyperactivity disorder; autism spectrum disorders; executive function; development; inhibition; flexibility; planning ID DIFFICULTIES QUESTIONNAIRE; COGNITIVE ESTIMATION; READING-DISABILITY; JOINT ATTENTION; YOUNG-CHILDREN; INDIVIDUALS; MIND; HYPERACTIVITY; COMORBIDITY; PERFORMANCE AB Deficits in 'executive function' (EF) are characteristic of several clinical disorders, most notably Autism Spectrum Disorders (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD). In this study, age- and IQ-matched groups with ASD, ADHD, or typical development (TD) were compared on a battery of EF tasks tapping three core domains: response selection/inhibition, flexibility, and planning/working memory. Relations between EF, age and everyday difficulties (rated by parents and teachers) were also examined. Both clinical groups showed significant EF impairments compared with TD peers. The ADHD group showed greater inhibitory problems on a Go-no-Go task, while the ASD group was significantly worse on response selection/monitoring in a cognitive estimates task. Age-related improvements were clearer in ASD and TD than in ADHD. At older (but not younger) ages, the ASD group outperformed the ADHD group, performing as well as the TD group on many EF measures. EF scores were related to specific aspects of communicative and social adaptation, and negatively correlated with hyperactivity in ASD and TD. Within the present groups, the overall findings suggested less severe and persistent EF deficits in ASD (including Asperger Syndrome) than in ADHD. (c) 2006 Elsevier Inc. All rights reserved. C1 Kings Coll London, MRC, Inst Psychiat, Social Genet & Dev Psychiat Ctr, London WC2B 5RL, England. Univ London, St Georges, Ctr Clin Neurosci, London, England. Univ Cambridge, Ctr Family Res, Cambridge CB2 1TN, England. RP Happe, F (reprint author), Kings Coll London, MRC, Inst Psychiat, Social Genet & Dev Psychiat Ctr, London WC2B 5RL, England. 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PD JUN PY 2006 VL 61 IS 1 BP 25 EP 39 DI 10.1016/j.bandc.2006.03.004 PG 15 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600004 PM 16682102 ER PT J AU Klin, A Jones, W AF Klin, A Jones, W TI Attributing social and physical meaning to ambiguous visual displays in individuals with higher-functioning autism spectrum disorders SO BRAIN AND COGNITION LA English DT Article DE autism; weak central coherence; social attribution; physical attribution ID ASPERGER-SYNDROME; CENTRAL COHERENCE; COGNITIVE DEFICIT; BRAIN; MIND; CHILDREN; INFORMATION; COMPREHENSION; MECHANISMS; PHENOTYPE AB The weak central coherence (WCC) account of autism characterizes the learning style of individuals with this condition as favoring localized and fragmented (to the detriment of global and integrative) processing of information. This pattern of learning is thought to lead to deficits in aspects of perception (e.g., face processing), cognition, and communication (e.g., focus on disjointed details rather than "gist" or context), ultimately leading to social impairments. This study was carried out to examine whether WCC applies to social and to non-social aspects of learning alike, or, alternatively, some areas of learning (e.g., physical reasoning) are spared in autism. Heider and Simmel's (1944) classic social animation as quantified in the Social Attribution Task (SAT) (Klin, 2000) and a novel animation involving physical reasoning (the Physical Attribution Task; PAT) were used to test the domain specificity of the WCC hypothesis. A pilot study involving a reference group of typically developing young adults and a group of individuals with higher-functioning autism spectrum disorders (ASDs) revealed gender differences in the reference group in regards to performance on the PAT (males outperformed females). In a follow-up case-control comparison involving only males where the ASD group was matched on age and IQ to a typically developing (TD) group of children, adolescents, and adults, the ASD group showed lower SAT scores and comparable PAT scores relative to the TD group. The interaction of diagnostic group by task was highly significant, with little overlap between the groups in the distributions of SAT minus PAT scores. These results indicated preserved integrative skills in the area of physical attribution in the ASD group, thus failing to support the WCC account as a domain-independent (or more general) model of learning in autism, while highlighting the centrality of the social deficits in the characterization of learning style in the autism spectrum disorders. (c) 2006 Published by Elsevier Inc. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Klin, A (reprint author), Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. 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This study investigated brain activation patterns using functional magnetic resonance imaging in right-handed adult males with ASD and a control group, matched on age, handedness, and verbal IQ. Semantic processing in the controls produced robust activation in Broca's area (left inferior frontal gyrus) and in superior medial frontal gyrus and right cerebellum. The ASD group had substantially reduced Broca's activation, but increased left temporal (Wernicke's) activation. Furthermore, the ASD group showed diminished activation differences between concrete and abstract words, consistent with behavioral studies. The current study suggests Broca's area is a region of abnormal neurodevelopment in ASD, which may be linked with semantic and related language deficits frequently observed in ASD. (c) 2006 Elsevier Inc. All rights reserved. C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA. 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PD JUN PY 2006 VL 61 IS 1 BP 54 EP 68 DI 10.1016/j.bandc.2005.12.015 PG 15 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600006 PM 16473449 ER PT J AU White, S Hill, E Winston, J Frith, U AF White, Sarah Hill, Elisabeth Winston, Joel Frith, Uta TI An islet of social ability in Asperger Syndrome: Judging social attributes from faces SO BRAIN AND COGNITION LA English DT Article DE Asperger Syndrome; social cognition; mentalizing; theory of mind; face recognition; stereotypes; attractiveness; trustworthiness; status ID HIGH-FUNCTIONING AUTISM; NORMAL ADULTS; MIND; CHILDREN; ATTRACTIVENESS; INDIVIDUALS; RECOGNITION; IMPAIRMENT; EMOTIONS; DISORDER AB We asked adults with Asperger Syndrome to judge pictorial stimuli in terms of certain social stereotypes to evaluate to what extent they have access to this type of social knowledge. Sixteen adults with Asperger Syndrome and 24 controls, matched for age and intelligence, were presented with sets of faces, bodies and objects, which had to be rated on a 7-point scale in terms of trustworthiness, attractiveness, social status, and age, or, in the case of objects, price. Despite impaired performance on two important aspects of social cognition (second-order mentalizing and face recognition) the social judgements of the individuals with Asperger Syndrome were just as competent and consistent as those of their matched controls, with only one exception: there was a trend for them to be less able to judge the attractiveness of faces if they were the same sex. We explain this difference in terms of a weakness in mentalizing, specifically the ability to take a different point of view: While all other stereotypic attributions could be made from an egocentric point of view, judging the attractiveness of faces of one's own sex requires taking the perspective of someone of the opposite sex, a challenge for people with mentalizing problems. We conclude that individuals with Asperger Syndrome show preserved aspects of social knowledge, as revealed in the attribution of stereotypes to pictures of people. These findings suggest that there are dissociable subcomponents to social cognition and that not all of these are compromised in Asperger Syndrome. (c) 2006 Elsevier Inc. All rights reserved. C1 UCL, Inst Cognit Neurosci, London, England. Univ London Goldsmiths Coll, London SE14 6NW, England. UCL, Wellcome Dept Imaging Neurosci, London, England. RP Frith, U (reprint author), UCL, Inst Cognit Neurosci, London, England. 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PD JUN PY 2006 VL 61 IS 1 BP 69 EP 77 DI 10.1016/j.bande.2005.12.007 PG 9 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600007 PM 16458402 ER PT J AU Ashwin, C Wheelwright, S Baron-Cohen, S AF Ashwin, C Wheelwright, S Baron-Cohen, S TI Finding a face in the crowd: Testing the anger superiority effect in Asperger Syndrome SO BRAIN AND COGNITION LA English DT Article DE Asperger Syndrome; autism; face-processing; visual search; emotions; amygdala ID BILATERAL AMYGDALA DAMAGE; FACIAL EXPRESSIONS; VISUAL-SEARCH; ENHANCED DISCRIMINATION; FUNCTIONING AUTISM; NORMAL ADULTS; RECOGNITION; FEAR; EMOTION; PERCEPTION AB Social threat captures attention and is processed rapidly and efficiently, with many lines of research showing involvement of the amygdala. Visual search paradigms looking at social threat have shown angry faces 'pop-out' in a crowd, compared to happy faces. Autism and Asperger Syndrome (AS) are neurodevelopmental conditions characterised by social deficits, abnormal face processing, and amygdala dysfunction. We tested adults with high-functioning autism (HFA) and AS using a facial visual search paradigm with schematic neutral and emotional faces. We found, contrary to predictions, that people with HFA/AS performed similarly to controls in many conditions. However, the effect was reduced in the HFA/AS group when using widely varying crowd sizes and when faces were inverted, suggesting a difference in face-processing style may be evident even with simple schematic faces. We conclude there are intact threat detection mechanisms in AS, under simple and predictable conditions, but that like other face-perception tasks, the visual search of threat faces task reveals atypical face-processing in HFA/AS. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. 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PD JUN PY 2006 VL 61 IS 1 BP 78 EP 95 DI 10.1016/j.bandc.2005.12.008 PG 18 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600008 PM 16455174 ER PT J AU Henderson, H Schwartz, C Mundy, P Burnette, C Sutton, S Zahka, N Pradella, A AF Henderson, H Schwartz, C Mundy, P Burnette, C Sutton, S Zahka, N Pradella, A TI Response monitoring, the error-related negativity, and differences in social behavior in autism SO BRAIN AND COGNITION LA English DT Article DE autism; response monitoring; error-related negativity; phenotypic variability ID HIGH-FUNCTIONING AUTISM; OBSESSIVE-COMPULSIVE DISORDER; ANTERIOR CINGULATE CORTEX; MEDIAL-FRONTAL-CORTEX; ASPERGER-SYNDROME; DEVELOPMENTAL PSYCHOPATHOLOGY; SPECTRUM DISORDERS; CHILDHOOD AUTISM; SCREENING QUESTIONNAIRE; BIOLOGICAL BASIS AB Children with autism not only display social impairments but also significant individual differences in social development. Understanding the source of these differences, as well as the nature of social impairments, is important for improved diagnosis and treatments for these children. Current theory and research suggests that individual differences in response monitoring, a specific function of the anterior cingulate cortex (ACC), may contribute to social-emotional and social-cognitive impairments and individual differences in autism. To examine this hypothesis, we used a modified flanker task to assess an ERP index of response monitoring, the error-related negativity (ERN), in a sample of higher function children with autism (HFA) and an IQ-matched control sample. The results revealed a significant Diagnostic group by Verbal IQ interaction on ERN amplitude indicating that the most verbally capable HFA children displayed significantly larger ERN amplitudes than did the control children. Within the HFA sample, greater ERN amplitude was also related to parent reports of fewer symptoms of social interaction impairments, fewer internalizing problems, but more externalizing problems, although these associations were reduced to nonsignificance when medication status was controlled. The latter results complement previous observations from imaging studies of a significant association between ACC activity and social symptoms and impairments in autism. The implications of these results for future research on brain-behavior relations, as well as treatment related research with children with autism are discussed. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Miami, Dept Psychol, Coral Gables, FL 33146 USA. RP Henderson, H (reprint author), Univ Miami, Dept Psychol, 5665 Ponce De Leon Blvd, Coral Gables, FL 33146 USA. 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PD JUN PY 2006 VL 61 IS 1 BP 96 EP 109 DI 10.1016/j.bandc.2005.12.009 PG 14 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600009 PM 16458401 ER PT J AU Belmonte, MK Carper, RA AF Belmonte, MK Carper, RA TI Monozygotic twins with Asperger syndrome: Differences in behaviour reflect variations in brain structure and function SO BRAIN AND COGNITION LA English DT Article DE autism-spectrum disorders; monozygotic twins; genetics; fMRI; MRI; morphometry ID EVENT-RELATED FMRI; ANTERIOR CINGULATE CORTEX; AUTISM SPECTRUM DISORDER; INFANTILE-AUTISM; CHILDREN; CONNECTIVITY; ATTENTION; MRI; CEREBELLUM; PERCEPTION AB A pair of monozygotic twins discordant for symptoms of Asperger syndrome was evaluated at the age of 13.45 years using psychometric, morphometric, behavioural, and functional imaging methods. The lower-functioning twin had a smaller brain overall, a smaller right cerebellum, and a disproportionately large left frontal lobe, and manifested almost no differential activation between distractors of high and low-congruence with target visual stimuli. The higher-functioning twin manifested a typically autistic pattern of anterior deactivation and posterior hyperactivation in response to incongruent distractors, overlaid with a typically normal pattern of activation of superior frontal cortex. The morphometric results are consistent with known correlations between brain structure and behaviour in autism, and the physiological results suggest correspondences between structure and function. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England. Childrens Hosp, Lab Res Neurosci Autism, San Diego, CA USA. Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA. RP Belmonte, MK (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England. 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PD JUN PY 2006 VL 61 IS 1 BP 110 EP 121 DI 10.1016/j.bandc.2005.12.010 PG 12 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600010 PM 16459007 ER PT J AU Baron-Cohen, S Ring, H Chitnis, X Wheelwright, S Gregory, L Williams, S Brammer, M Bullmore, ET AF Baron-Cohen, Simon Ring, Howard Chitnis, Xavier Wheelwright, Sally Gregory, Lloyd Williams, Steve Brammer, Mick Bullmore, Edward T. TI fMRI of parents of children with Asperger Syndrome: A pilot study SO BRAIN AND COGNITION LA English DT Article DE autism; Asperger Syndrome; fMRI parents; sex differences ID AUTISM-SPECTRUM QUOTIENT; FUNCTIONING AUTISM; BRAIN; PERMUTATION; ADULTS; TESTS; MIND AB Background: People with autism or Asperger Syndrome (AS) show altered patterns of brain activity during visual search and emotion recognition tasks. Autism and AS are genetic conditions and parents may show the 'broader autism phenotype.' Aims: (1) To test if parents of children with AS show atypical brain activity during a visual search and an empathy task; (2) to test for sex differences during these tasks at the neural level; (3) to test if parents of children with autism are hyper-masculinized, as might be predicted by the 'extreme male brain' theory. Method: We used fMRI during a visual search task (the Embedded Figures Test (EFT)) and an emotion recognition test (the 'Reading the Mind in the Eyes' (or Eyes) test). Sample: Twelve parents of children with AS, vs. 12 sex-matched controls. Design: Factorial analysis was used to map main effects of sex, group (parents vs. controls), and sex x group interaction on brain function. An ordinal ANOVA also tested for regions of brain activity where females > males > fathers = mothers, to test for parental hyper-masculinization. Results on EFT task: Female controls showed more activity in extrastriate cortex than male controls, and both mothers and fathers showed even less activity in this area than sex-matched controls. There were no differences in group activation between mothers and fathers of children with AS. The ordinal ANOVA identified two specific regions in visual cortex (right and left, respectively) that showed the pattern Females > Males > Fathers = Mothers, both in BA 19. Results on Eyes task: Male controls showed more activity in the left inferior frontal gyrus than female controls, and both mothers and fathers showed even more activity in this area compared to sex-matched controls. Female controls showed greater bilateral inferior frontal activation than males. This was not seen when comparing mothers to males, or mothers to fathers. The ordinal ANOVA identified two specific regions that showed the pattern Females > Males > Mothers = Fathers: left medial temporal gyrus (BA 21) and left dorsolateral prefrontal cortex (BA 44). Conclusions: Parents of children with AS show atypical brain function during both visual search and emotion recognition, in the direction of hyper-masculinization of the brain. Because of the small sample size, and lack of age-matching between parents and controls, such results constitute a pilot study that needs replicating with larger samples. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. Univ London, MRI Unit, Inst Psychiat, London SE5 8AF, England. Univ Cambridge, Addenbrookes Hosp, Sch Clin, Dept Psychiat,Brain Mappint Unit, Cambridge CB2 2QQ, England. Hope Hosp, Translat Imaging Unit, Salford M6 8HD, Lancs, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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PD JUN PY 2006 VL 61 IS 1 BP 122 EP 130 DI 10.1016/j.bandc.2005.12.011 PG 9 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 054MZ UT WOS:000238382600011 PM 16460858 ER PT J AU Marchant, P Hussain, A Hall, K AF Marchant, P Hussain, A Hall, K TI Autistic Spectrum Disorders and Asian children SO BRITISH JOURNAL OF EDUCATIONAL STUDIES LA English DT Article DE autism; autistic spectrum disorder; ASD; prevalence ID CHILDHOOD AUTISM; DIAGNOSIS; ACCOUNT; MIND AB This paper compares the incidence of the diagnosis of Autistic Spectrum Disorders (ASD) among White and Asian children with reference to data obtained from thirteen local education authorities (LEAs) in England. It begins by outlining some of the theoretical debates associated with the definition, diagnosis and prevalence of ASD. 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L., 1990, MIMESIS MAKE BELIEVE Williams E, 2001, J AUTISM DEV DISORD, V31, P67, DOI 10.1023/A:1005665714197 NR 62 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1389-0417 J9 COGN SYST RES JI Cogn. Syst. Res. PD JUN PY 2006 VL 7 IS 2-3 BP 113 EP 127 DI 10.1016/j.cogsys.2005.11.008 PG 15 WC Computer Science, Artificial Intelligence; Neurosciences; Psychology, Experimental SC Computer Science; Neurosciences & Neurology; Psychology GA 113VO UT WOS:000242626300003 ER PT J AU Pelphrey, KA Morris, JP AF Pelphrey, KA Morris, JP TI Brain mechanisms for interpreting the actions of others from biological-motion cues SO CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE LA English DT Article DE social perception; social cognition; superior temporal sulcus region; functional neuroimaging; autism ID SUPERIOR TEMPORAL SULCUS; SOCIAL-PERCEPTION; GAZE SHIFTS; CORTEX; EYE; ACTIVATION; AMYGDALA; AUTISM; FACES AB Humans are an intensely social species. Our social abilities depend upon specialized brain systems for rapidly recognizing the faces of others, for interpreting the actions of others through an analysis of biological-motion cues, and for determining the emotional states of others via inspection of facial expression. Recent work has implicated the superior temporal sulcus (STS) region as an important component of the social brain. Functional neuroimaging studies have provided clues about how this region is involved in the visual analysis and interpretation of other people's actions. STS activity is modulated by the context within which the actions of biological entities are observed. Such a contextual influence is consistent with a broader tradition within social psychology emphasizing the powerful influences of situational and contextual factors on behavior and perception. The STS region also shows promise as a region of importance in the investigation of both typical and impaired social-cognitive development. Future work should aim to inform us better of the development of interrelationships between the STS region and other regions of the social brain, including the amygdala and the fusiform gyrus. C1 Duke Univ, Durham, NC 27708 USA. RP Pelphrey, KA (reprint author), Duke Univ, 9 Flowers Dr, Durham, NC 27708 USA. 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MECP2 mutations have also been identified in individuals with a variety of clinical syndromes, including mild learning-disability in females, neonatal encephalopathy in males, and psychiatric disorders, autism and X-linked mental retardation in both males and females. Furthermore, MECP2 duplications have been shown to cause a progressive postnatal neurological disorder. MeCP2 is a transcriptional repressor that binds to methylated CpG dinucleotides flanked by AT-rich segments and recruits a corepressor complex, thereby altering chromatin structure. Subtle gene expression changes have been identified in Rett patients and mouse models; however, MeCP2 dysfunction has also been shown to cause abnormalities of RNA splicing, suggesting a complex molecular pathogenesis. Discovering which genes are misregulated in the absence of functional MeCP2 and demonstrating their role in causing neuronal dysfunction and disease manifestations are challenging but important steps for understanding the pathogenesis of Rett syndrome and related disorders. C1 Baylor Coll Med, Houston, TX 77030 USA. RP Zoghbi, HY (reprint author), Baylor Coll Med, 1 Baylor Plaza,T807,Mail Stop 225, Houston, TX 77030 USA. 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Opin. Genet. Dev. PD JUN PY 2006 VL 16 IS 3 BP 276 EP 281 DI 10.1016/j.gde.2006.04.009 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 054BP UT WOS:000238350900011 PM 16647848 ER PT J AU Post, JN AF Post, Jennifer N. TI Immunizations, neonatal jaundice and animal-induced injuries SO CURRENT OPINION IN PEDIATRICS LA English DT Review DE animal bites; hyperbilirubinemia; immunizations; jaundice ID UNITED-STATES; VACCINATION STRATEGIES; VARICELLA OUTBREAK; COST-EFFECTIVENESS; PERTUSSIS-VACCINE; DOUBLE-BLIND; HYPERBILIRUBINEMIA; ADOLESCENTS; NEWBORNS; EFFICACY AB Purpose of review To review the literature published within the last year on three topics essential to clinical pediatrics: immunizations, neonatal jaundice, and animal-induced injuries. Recent findings New vaccines that protect against meningococcus, pertussis and rotavirus are safe, effective and recommended for routine immunization. Young children remain a high priority for influenza vaccination while the world awaits further developments of avian influenza. Pneumococcal and varicella vaccinations have benefited many. Debate exists on how to screen for hyperbilirubinemia in neonates and new strategies are emerging to prevent it. There seems to be no link between hyperbilirubinemia and autism spectrum disorders. We have learned that rabies can be transmitted by transplantation; it remains a global public health problem and its incidence is frequently underestimated in developing nations. Lastly, brown recluse spider bites are often misdiagnosed. Summary The face of pediatric infectious disease is changing as we incorporate new vaccines into our routine practice. Rotavirus vaccine has significant implications for the health of children across the globe. The management strategy for neonatal jaundice continues to focus on screening and prevention. We need to devote more energy to combating rabies in countries where it is endemic. C1 Harvard Univ, Sch Med, Childrens Hosp, Primary Care Ctr, Boston, MA 02115 USA. RP Post, JN (reprint author), Harvard Univ, Sch Med, Childrens Hosp, Primary Care Ctr, 300 Longwood Ave, Boston, MA 02115 USA. 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PD JUN PY 2006 VL 18 IS 3 BP 330 EP 335 DI 10.1097/01.mop.0000193315.52957.e3 PG 6 WC Pediatrics SC Pediatrics GA V63FM UT WOS:000204273000019 PM 16721158 ER PT J AU Glogowska, M Roulstone, S Peters, TJ Enderby, P AF Glogowska, M Roulstone, S Peters, TJ Enderby, P TI Early speech- and language-impaired children: linguistic, literacy, and social outcomes SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PRESCHOOL-CHILDREN; RETARDATION; DELAY AB The aim of this study was to follow-up prospectively a cohort of preschool children originally recruited from successive referrals to speech and language therapy community clinics and to investigate their linguistic, literacy, and social outcomes at 7 to 10 years of age. Three hundred and fifty children aged 84 to 113 months (mean age 99.9mo [SD 5.4mo]) were singletons from monolingual backgrounds where there was concern about their speech and language development. Children who had severe learning difficulties, autism, oromotor deficits, dysfluency, or dysphonia were excluded. Altogether 196 (56%), 134 males and 62 females, were seen at follow-up. A control group of children who had never been referred for speech and language therapy, 57% of whom were males, was also recruited (n=94; mean age 104.4mo [SD 6.8mo]). All children were assessed on standardized measures of speech, language, and literacy. Teachers and parents completed questionnaires on educational and social outcomes. In total, 139 children in the cohort were within the normal range on standardized language assessments. About 30% of the original cohort of children continue to struggle with language, literacy, and social difficulties. The study demonstrates the long-term nature of language impairment and reinforces the need for awareness among professionals in child development and education of the ongoing needs of this population of children. C1 Frenchay Hosp, Speech & Language Therapy Res Unit, Bristol BS16 1LE, Avon, England. Univ W England, Fac Hlth & Social Care, Bristol BS16 1QY, Avon, England. Univ Bristol, Dept Community Based Med, Bristol, Avon, England. Univ Sheffield, Inst Gen Practice & Primary Care, Sheffield, S Yorkshire, England. RP Roulstone, S (reprint author), Frenchay Hosp, Speech & Language Therapy Res Unit, Bristol BS16 1LE, Avon, England. EM sue@speech-therapy.org.uk CR BISHOP DVM, 1990, J CHILD PSYCHOL PSYC, V31, P1027, DOI 10.1111/j.1469-7610.1990.tb00844.x Bishop D. V. M., 1989, TEST RECEPTION GRAMM BISHOP DVM, 1987, J SPEECH HEAR DISORD, V52, P156 Fundudis T, 1979, SPEECH RETARDED DEAF Gathercole S. 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S., 1993, WIDE RANGE ACHIEVEME NR 23 TC 13 Z9 13 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD JUN PY 2006 VL 48 IS 6 BP 489 EP 494 DI 10.1017/S0012162206001046 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 050BI UT WOS:000238062100017 PM 16700942 ER PT J AU Wier, ML Yoshida, CK Odonli, R Grether, JK Croen, LA AF Wier, ML Yoshida, CK Odonli, R Grether, JK Croen, LA TI Congenital anomalies associated with autism spectrum disorders SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID HYPERTROPHIC PYLORIC-STENOSIS; BIRTH-DEFECTS; DEVELOPMENTAL-DISABILITIES; POSTNATAL FACTORS; CHILDHOOD AUTISM; RISK-FACTORS; POPULATION; EPIDEMIOLOGY; CHILDREN; COMPLICATIONS AB This study examined whether major congenital structural anomalies identified in infancy occurred more frequently in children later diagnosed with autism spectrum disorders (ASD; n=417; 341 males, 76 females) than in comparison children (n=2067; 1681 males, 386 females). Participants were sampled from infants born at Kaiser Permanente Northern California facilities between 1995 and 1999 who remained health plan members for at least 2 years (n=88 163). Comparison children were frequency-matched to children with ASD according to sex, birth year, and birth hospital. Congenital anomalies were diagnosed in 10.8% of children with ASD and 6.2% of comparison children (crude odds ratio [ORc] 1.8, 95% confidence interval [CI] 1.3-2.6). This association remained significant after adjustment for key maternal and infant covariates (adjusted OR [ORa] 1.7, 95% CI 1.1-2.4). Almost all organ-system anomaly categories were more prevalent in children with ASD, however only gastrointestinal anomalies were significantly associated with ASD in adjusted analyses (1.9 vs 0.4%, ORa 5.1, 95% CI 1.8-14.1). C1 Kaiser Permanente, Div Res, Oakland, CA 94612 USA. Dept Hlth Serv, Environm Hlth Invest Branch, Richmond, CA USA. RP Croen, LA (reprint author), Kaiser Permanente, Div Res, 2000 Broadway, Oakland, CA 94612 USA. EM Lisa.A.Croen@kp.org CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT BRENNER WE, 1976, AM J OBSTET GYNECOL, V126, P555 *CAL BIRTH DEF MON, 2004, COMM SER BIRTH DEF S Croen LA, 2002, J AUTISM DEV DISORD, V32, P217, DOI 10.1023/A:1015405914950 Croen L A, 1991, Paediatr Perinat Epidemiol, V5, P423, DOI 10.1111/j.1365-3016.1991.tb00728.x DEYKIN EY, 1980, AM J DIS CHILD, V134, P860 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Hultman CM, 2002, EPIDEMIOLOGY, V13, P417, DOI 10.1097/01.EDE.0000016968.14007.E6 James WH, 2004, BIRTH DEFECTS RES A, V70, P37, DOI 10.1002/bdra.10097 Jelliffe-Pawlowski LL, 2003, ARCH PEDIAT ADOL MED, V157, P545, DOI 10.1001/archpedi.157.6.545 Juul-Dam N, 2001, PEDIATRICS, V107, part. no., DOI 10.1542/peds.107.4.e63 KHOURY MJ, 1989, EPIDEMIOL REV, V11, P244 Kirby RS, 2002, MENT RETARD DEV D R, V8, P182, DOI 10.1002/mrdd.10034 KRIEGER N, 1992, AM J PUBLIC HEALTH, V82, P703, DOI 10.2105/AJPH.82.5.703 Lary JM, 2001, TERATOLOGY, V64, P237, DOI 10.1002/tera.1070 LAURITSEN MB, 2000, J AUTISM DEVEL DISOR, V32, P115 LECOUTEUR A, 2003, AUTISM DIAGNOSTIC IN LINKS PS, 1980, J AUTISM DEV DISORD, V10, P273, DOI 10.1007/BF02408286 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 MASONBROTHERS A, 1990, PEDIATRICS, V86, P514 MASONBROTHERS A, 1987, J AM ACAD CHILD PSY, V26, P39, DOI 10.1097/00004583-198701000-00008 Newschaffer CJ, 2002, EPIDEMIOL REV, V24, P137, DOI 10.1093/epirev.mxf010 Pisacane A, 1996, BRIT MED J, V312, P745 *PRACT MAN INF COR, 1999, INT CLASS DIS 9 REV Rice C, 2004, AM J MED GENET C, V125C, P22, DOI 10.1002/ajmg.c.30006 Rodier PM, 1997, TERATOLOGY, V55, P319, DOI 10.1002/(SICI)1096-9926(199705)55:5<319::AID-TERA4>3.0.CO;2-U Schechter R, 1997, PAEDIATR PERINAT EP, V11, P407, DOI 10.1046/j.1365-3016.1997.d01-32.x SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 STROMLAND K, 1994, DEV MED CHILD NEUROL, V36, P351 WALKER HA, 1977, J AUTISM CHILD SCHIZ, V7, P165, DOI 10.1007/BF01537727 WHO, 1967, MAN INT STAT CLASS D World Health Organization, 1977, MAN INT STAT CLASS D Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 34 TC 24 Z9 25 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD JUN PY 2006 VL 48 IS 6 BP 500 EP 507 DI 10.1017/S001216220600106X PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 050BI UT WOS:000238062100019 PM 16700944 ER PT J AU Gravel, JS Dunn, M Lee, WW Ellis, MA AF Gravel, JS Dunn, M Lee, WW Ellis, MA TI Peripheral audition of children on the autistic spectrum SO EAR AND HEARING LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; AUDITORY-EVOKED-POTENTIALS; BRAIN-STEM RESPONSES; LANGUAGE DISORDER; OTITIS-MEDIA; HEARING-LOSS; DIAGNOSTIC INTERVIEW; INFANTILE-AUTISM; ABNORMALITIES; DYSFUNCTION AB Objective: To determine whether the peripheral audition of a group of children comprehensively diagnosed as being on the autistic spectrum was quantitatively different from that of a matched group of typically developing children. Methods: Thirty-seven children with autism and an equal number of control participants matched for chronological age within 6 mo were examined by means of behavioral and physiologic measures of auditory function. All participants had normal hearing (thresholds < 15 dB HL; 0.25 to 8 kHz) and normal middle ear function by quantitative tympanometry. Conventional behavioral audiometry, a computer-assisted threshold assessment procedure, acoustic middle ear muscle reflex thresholds, and evoked otoacoustic emissions (both transient and distortion product) tests were administered to both groups. Results: No significant differences between children with autism and those developing typically on any behavioral or physiologic measure of peripheral auditory function were found. Conclusions: There was no evidence of intrinsic differences in the peripheral auditory mechanism of children with autism that would account for the auditory processing disorders and sound sensitivity that are commonly reported in this population. C1 Childrens Hosp Philadelphia, Ctr Childhood Commun, Philadelphia, PA 19104 USA. Albert Einstein Coll Med, Rose F Kennedy Ctr, Bronx, NY 10467 USA. RP Gravel, JS (reprint author), Childrens Hosp Philadelphia, Ctr Childhood Commun, Childrens Seashore House,Room 113,3405 Civ Ctr Bl, Philadelphia, PA 19104 USA. 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PD JUN PY 2006 VL 27 IS 3 BP 299 EP 312 DI 10.1097/01.aud.0000215979.65645.22 PG 14 WC Audiology & Speech-Language Pathology; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Otorhinolaryngology GA 041GB UT WOS:000237441200009 PM 16672798 ER PT J AU Tincani, M Crozier, S Alazetta, L AF Tincani, M Crozier, S Alazetta, L TI The picture exchange communication system: Effects on manding and speech development for school-aged children with autism SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID DISABILITIES; PECS AB We examined the effects of the Picture Exchange Communication System (PECS; Frost & Bondy, 2002) on the manding (requesting) and speech development of school-aged children with autism. In study 1, two participants, Damian and Bob, were taught PECS within a delayed multiple baseline design. Both participants demonstrated increased levels of manding after implementation of PECS. Only Damian demonstrated any measurable speech during study 1. His speech development occurred primarily during phase IV of PECS. Because of the positive relationship between Phase IV and increased speech,for Damian, study 2 was conducted to confirm a functional relationship between phase IV procedures and speech development for an additional participant. Carl received phase TV training procedures in two conditions, administered in an ABAB design. In condition A, no reinforcement was provided for vocalization; in condition B, reinforcement was provided for vocalization after a delay of 3- to 5-s. The vocal reinforcement procedures in phase B differentially increased Carls speech. Results are discussed in terms Of research on augmentative and alternative communication and speech development for children with autism. C1 Univ Nevada, Dept Special Educ, Las Vegas, NV 89154 USA. RP Tincani, M (reprint author), Univ Nevada, Dept Special Educ, 4505 Maryland Pkwy,Box 453014, Las Vegas, NV 89154 USA. EM tincanim@unlv.nevada.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bondy A. S., 1994, FOCUS AUTISTIC BEHAV, V9, P1, DOI DOI 10.1177/108835769400900301 Charlop-Christy MH, 2002, J APPL BEHAV ANAL, V35, P213, DOI 10.1901/jaba.2002.35-213 Cooper J., 1987, APPL BEHAV ANAL Durand V. 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Disabil. PD JUN PY 2006 VL 41 IS 2 BP 177 EP 184 PG 8 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 052MP UT WOS:000238238100007 ER PT J AU Santosh, PJ Mijovic, A AF Santosh, PJ Mijovic, A TI Does pervasive developmental disorder protect children and adolescents against drug and alcohol use? SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE PDD; autism; alcohol; drug ID SUBSTANCE USE DISORDER; PSYCHIATRIC-DISORDERS; RISK-FACTORS; COMORBIDITY; PREVALENCE; MECHANISMS; AUTISM; ABUSE; ONSET; ADHD AB Aim The aim of this paper is (1) to compare the rates of reported drug and/or alcohol use (DAU) in treatment seeking adolescents with Pervasive Developmental Disorders (PDD), and those with other psychiatric diagnoses (psychiatric controls) seen in tertiary child and adolescent mental health services and (2) to explore the relationship of psychopathology, environmental stressors, and social communication difficulties to DAU. Method Data from the chart review of children and adolescents aged between 12 and 18 years with psychiatric diagnosis seen in tertiary child and adolescent mental health services between 1992 and 2001 (n=1484) was used to investigate the relationship between DAU, psychopathology, environmental stressors and items related to social communication. Results A total of 97 subjects (7%) met criteria for PDD. Subjects with PDD report significantly lower DAU than psychiatric controls, 3% vs. 17% respectively (P < 0.000). Factors reflecting PDD such as speech and language difficulties, developmental difficulties, discordant peer relationships in adolescents are negatively associated with DAU, while conduct problems, affective symptoms, inadequate parental supervision or control have positive association with DAU. DAU was present in PDD only when comorbid with Attention Deficit Hyperactivity Disorder (ADHD). Conclusion Adolescents with speech and language difficulties, developmental difficulties and discordant peer relationships, all reflecting PDD, are less likely to have DAU. C1 Great Ormond St Hosp Children, Dept Child & Adolescent Mental Hlth, London WC1N 3JH, England. Inst Child Hlth, London, England. Inst Psychiat, London, England. St Georges Child & Adolescent Higher Training Sch, London, England. RP Santosh, PJ (reprint author), Great Ormond St Hosp Children, Dept Child & Adolescent Mental Hlth, Great Ormond St, London WC1N 3JH, England. EM SantoP@gosh.nhs.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BENJAMIN J, 1996, NAT GENET, V12, P8184 Biederman J, 1997, J AM ACAD CHILD PSY, V36, P21, DOI 10.1097/00004583-199701000-00013 BUKSTEIN OG, 1989, AM J PSYCHIAT, V146, P1131 CLONINGER CR, 1987, SCIENCE, V236, P410, DOI 10.1126/science.2882604 Crowley T J, 1995, NIDA Res Monogr, V156, P49 Ebstein RP, 1996, NAT GENET, V12, P78, DOI 10.1038/ng0196-78 FERGUSSON DM, 1995, ADDICTION, V90, P935, DOI 10.1111/j.1360-0443.1995.tb03502.x GOODMAN R, 1991, J CHILD PSYCHOL PSYC, V32, P551, DOI 10.1111/j.1469-7610.1991.tb00331.x GREENBAUM PE, 1991, J AM ACAD CHILD PSY, V30, P575, DOI 10.1097/00004583-199107000-00008 KANDEL DB, 1978, J YOUTH ADOLESCENCE, V7, P13, DOI 10.1007/BF01538684 Kandel D B, 1985, Adv Alcohol Subst Abuse, V4, P139 KARNO M, 1988, ARCH GEN PSYCHIAT, V45, P1094 KASHANI JH, 1985, J AFFECT DISORDERS, V8, P153, DOI 10.1016/0165-0327(85)90038-2 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Masse LC, 1997, ARCH GEN PSYCHIAT, V54, P62 Rasmussen P, 2000, J AM ACAD CHILD PSY, V39, P1424, DOI 10.1097/00004583-200011000-00017 RASMUSSEN SA, 1988, PSYCHOPHARMACOL BULL, V24, P466 REEBYE P, 1995, CAN J PSYCHIAT, V40, P313 ROBINS L, 1981, ARCH GEN PSYCHIAT, V29, P766 Santosh PJ, 2004, EUR CHILD ADOLES PSY, V13, P141, DOI 10.1007/s00787-004-0372-4 Soderpalm B, 2002, EUR J PAIN-LONDON, V6, P3, DOI 10.1053/eujp.2001.0315 Swadi H, 1999, DRUG ALCOHOL DEPEN, V55, P209, DOI 10.1016/S0376-8716(99)00017-4 Tarter R, 1999, DEV PSYCHOPATHOL, V11, P657, DOI 10.1017/S0954579499002266 THORLEY G, 1982, J ADOLESCENCE, V5, P179, DOI 10.1016/S0140-1971(82)80046-8 Wang MQ, 1997, AM J HEALTH BEHAV, V21, P111 World Health Organization, 1996, MULT CLASS CHILD AD World Health Organization, 1992, INT CLASS DIS NR 29 TC 10 Z9 11 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD JUN PY 2006 VL 15 IS 4 BP 183 EP 188 DI 10.1007/s00787-005-0517-0 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 047BO UT WOS:000237855000001 PM 16604379 ER PT J AU Lindquist, B Carlsson, G Persson, EK Uvebrant, P AF Lindquist, B Carlsson, G Persson, EK Uvebrant, P TI Behavioural problems and autism in children with hydrocephalus - A population-based study SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE behaviour; autism; hydrocephalus; myelomeningocele; children ID INFANTILE HYDROCEPHALUS; BRAIN-DAMAGE; FOLLOW-UP; DISORDERS; ADJUSTMENT; PREVALENCE; SEQUELAE; IMPACT; BORN AB Objective To investigate the prevalence of behavioural problems and autism in a population-based group of children with hydrocephalus and to see whether learning disabilities, cerebral palsy (CP), epilepsy, myelomeningocele (MMC) or preterm birth increase the risk of these problems. Method In the 107 children with hydrocephalus born in western Sweden in 1989-1993, behaviour was assessed using the Conners' parent rating scales in 66 and the teacher's rating scales in 57. Autism was investigated using the Childhood Autism Rating Scale. Results Parents rated 67% of the children and teachers 39% of the children as having behavioural problems (> 1.5 SD, or T score > 65). Learning disabilities increased the risk significantly and almost all the children with CP and/or epilepsy had behavioural problems. Autism was present in nine children (13%), in 20% of those without MMC and in one of 26 with MMC. Autism was significantly more frequent in children with learning disabilities (27% vs. 7%) and in children with CP and/or epilepsy (33% vs. 6%). Conclusion The majority of children with hydrocephalus have behavioural problems and many have autism. It is therefore important to assess and understand all the aspects of cognition and behaviour in these children in order to minimise disability and enhance participation for the child. C1 Univ Gothenburg, Queen Silvia Childrens Hosp, S-41685 Gothenburg, Sweden. Halmstad Cty Hosp, Dept Habilitat, S-0185 Halmstad, Sweden. Univ Schleswig Holstein, Dept Paediat, Kiel, Germany. RP Uvebrant, P (reprint author), Univ Gothenburg, Queen Silvia Childrens Hosp, S-41685 Gothenburg, Sweden. EM paul.uvebrant@pediat.gu.se CR American Psychiatric Association, DIAGN STAT MAN MENT BILENBERG N, 2001, EUR J PEDIAT SURG S1, V11, P544 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 CONNELL HM, 1981, DEV MED CHILD NEUROL, V23, P505 Conners C. 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Child Adolesc. Psych. PD JUN PY 2006 VL 15 IS 4 BP 214 EP 219 DI 10.1007/s00787-006-0525-8 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 047BO UT WOS:000237855000005 PM 16502210 ER PT J AU Klauck, SM AF Klauck, Sabine M. TI Genetics of autism spectrum disorder SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Review DE autism; whole-genome screens; susceptibility loci; candidate genes ID PERVASIVE DEVELOPMENTAL DISORDERS; GENOME-WIDE SCAN; SEROTONIN TRANSPORTER; REELIN GENE; LINKAGE-DISEQUILIBRIUM; SUSCEPTIBILITY LOCUS; NEUROLIGIN GENES; CHROMOSOME 7Q; COMPULSIVE BEHAVIORS; SAVANT SKILLS AB Autism is a highly heritable complex neurodevelopmental disorder characterized by distinct impairments of cognitive function in the field of social interaction and speech development. Different approaches have been undertaken worldwide to identify susceptibility loci or genes for autism spectrum disorders. No clear conclusions can be made today about genetic loci involved in these disorders. The review will focus on relevant results from the last decade of research with emphasis on whole genome screens and association studies. C1 Deutsch Krebsforschungszentrum, Div Mol Genome Anal, D-69120 Heidelberg, Germany. RP Klauck, SM (reprint author), Deutsch Krebsforschungszentrum, Div Mol Genome Anal, Neuenheimer Feld 580, D-69120 Heidelberg, Germany. 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J. Hum. Genet. PD JUN PY 2006 VL 14 IS 6 BP 714 EP 720 DI 10.1038/sj.ejhg.5201610 PG 7 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 046IY UT WOS:000237806400009 PM 16721407 ER PT J AU Palmer, RF Blanchard, S Stein, Z Mandell, D Miller, C AF Palmer, RF Blanchard, S Stein, Z Mandell, D Miller, C TI Environmental mercury release, special education rates, and autism disorder: an ecological study of Texas SO HEALTH & PLACE LA English DT Article DE mercury; special education; autism; environmental toxins; ecological ID NERVOUS-SYSTEM; METHYLMERCURY; EXPOSURE; LEAD; TOXICOLOGY; TOXICITY; TAGUM; STATE; MILK AB The association between environmentally released mercury, special education and autism rates in Texas was investigated using data from the Texas Education Department and the United States Environmental Protection Agency. A Poisson regression analysis adjusted for school district population size, economic and demographic factors was used. There was a significant increase in the rates of special education students and autism rates associated with increases in environmentally released mercury. On average, for each 1000 1b of environmentally released mercury, there was a 43% increase in the rate of special education services and a 61% increase in the rate of autism. The association between environmentally released mercury and special education rates were fully mediated by increased autism rates. This ecological study suggests the need for further research regarding the association between environmentally released mercury and developmental disorders such as autism. These results have implications for policy planning and cost analysis. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Texas, Hlth Sci Ctr, San Antonio Dept Family & Community Med, San Antonio, TX 78229 USA. 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There is growing evidence that testosterone exerts similar influences on human development, although the range of behaviors affected is not completely known. This study examined the hypothesis that autistic traits are increased following prenatal exposure to abnormally high levels of testosterone caused by congenital adrenal hyperplasia (CAH). Sixty individuals with CAH (34 female, 26 male) and 49 unaffected relatives (24 female, 25 male) completed the Autism Spectrum Quotient (AQ). Females with CAH scored significantly higher than unaffected females on total AQ score, largely due to enhanced scores on subscales measuring social skills and imagination. These results suggest that prenatal exposure to high levels of testosterone influences some autistic traits and that hormonal factors may be involved in vulnerability to autism. (c) 2006 Elsevier Inc. All rights reserved. C1 City Univ London, Dept Psychol, London EC1V 0HB, England. 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Behav. PD JUN PY 2006 VL 50 IS 1 BP 148 EP 153 DI 10.1016/j.yhbeh.2006.02.006 PG 6 WC Behavioral Sciences; Endocrinology & Metabolism SC Behavioral Sciences; Endocrinology & Metabolism GA 054QZ UT WOS:000238395000020 PM 16624315 ER PT J AU Liu, J Francke, U AF Liu, Jinglan Francke, Uta TI Identification of cis-regulatory elements for MECP2 expression SO HUMAN MOLECULAR GENETICS LA English DT Article ID CPG-BINDING PROTEIN; BZIP TRANSCRIPTION FACTOR; SEVERE MENTAL-RETARDATION; RETT-SYNDROME; INFANTILE SPASMS; DNA METHYLATION; GENE-EXPRESSION; MUTATIONS; CHROMATIN; DIFFERENTIATION AB Rett syndrome (RTT) is an X-linked dominant disabling neurodevelopmental disorder caused by loss of function mutations in the MECP2 gene, located at Xq28, which encodes a multifunctional protein. MECP2 expression is regulated in a developmental stage and cell-type-specific manner. The need for tightly controlled MeCP2 levels in brain is strongly suggested by neurologically abnormal phenotypes of mouse models with mild overexpression and by mental retardation in human males with MECP2 duplication. We set out to identify long-range cis-regulatory sequences that differentially regulate MECP2 transcription and, when mutated, may contribute to the pathogenesis of RTT, autism or X-linked mental retardation. By inter-species sequence comparisons, we detected 27 highly conserved non-coding DNA sequences within a 210 kb region covering MECP2. We functionally confirmed four enhancer and two silencer elements by performing luciferase reporter assays in four different human cell lines. The transcription factor binding capability of the identified regulatory elements was tested by gel shift assays. To locate the human MECP2 core promoter, we dissected the promoter region by reporter assays with deletion constructs. We then used chromosome conformation capture methods to document long-range interactions of three enhancers and two silencers with the MECP2 promoter. Acting over distances of up to 130 kb, these elements may influence chromatin configurations and regulate MECP2 transcription. Our study has defined the 'MECP2 functional expression module' and identified enhancer and silencer elements that are likely to be responsible for the tissue-specific, developmental stage-specific or splice-variant-specific control of MeCP2 protein expression. C1 Stanford Univ, Sch Med, Beckman Ctr Mol & Genet Med, Dept Genet, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA. RP Francke, U (reprint author), Stanford Univ, Sch Med, Beckman Ctr Mol & Genet Med, Dept Genet, 279 Campus Dr, Stanford, CA 94305 USA. 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Mol. Genet. PD JUN 1 PY 2006 VL 15 IS 11 BP 1769 EP 1782 DI 10.1093/hmg/ddl099 PG 14 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 044UA UT WOS:000237696700003 PM 16613900 ER PT J AU Passone, SM AF Passone, SM TI Autism : debates and testimonies SO INTERNATIONAL JOURNAL OF PSYCHOANALYSIS LA English DT Book Review RP Passone, SM (reprint author), 108bis,bd A Blanqui, F-75013 Paris, France. EM sesto.passone@psp.ucl.ac.be CR RIBAS D, 2005, AUTISM DEBATES TESTI RIBAS D, IN PRESS AUTISM DEBA NR 2 TC 0 Z9 0 PU INST PSYCHO-ANALYSIS PI LONDON PA BYRON HOUSE, 112A-114 SHIRLAND RD, LONDON W9 2EQD, ENGLAND SN 0020-7578 J9 INT J PSYCHOANAL JI Int. J. Psychoanal. PD JUN PY 2006 VL 87 BP 904 EP 906 PN 3 PG 3 WC Psychology, Psychoanalysis SC Psychology GA 058II UT WOS:000238658300030 ER PT J AU Goldsmith, HH Van Hulle, CA Arneson, CL Schreiber, JE Gernsbacher, MA AF Goldsmith, HH Van Hulle, CA Arneson, CL Schreiber, JE Gernsbacher, MA TI A population-based twin study of parentally reported tactile and auditory defensiveness in young children SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article DE sensory defensiveness; twins; temperament; genetics; anxiety ID FRAGILE-X-SYNDROME; ELECTRODERMAL RESPONSES; INDIVIDUAL-DIFFERENCES; SENSORY PROFILE; TEMPERAMENT; AUTISM; VALIDITY; TODDLER; QUESTIONNAIRE; PERFORMANCE AB Some adults and children exhibit defensive behaviors to tactile or auditory stimulation. These symptoms occur not only in subsets of children with ADHD, autism, and Fragile X syndrome, but also in the apparent absence of accompanying disorders. Relatively little research explores the correlates and antecedents of sensory defensiveness. Using a population-based sample of 1,394 toddler-aged twins, mothers reported on tactile and auditory defensiveness, temperament, and behavior problems. The incidence of defensive symptoms was widely distributed, with some accumulation of cases in the extreme range. Girls were overrepresented in the extreme tactile defensiveness group. Both auditory and tactile defensiveness were modestly associated with fearful temperament and anxiety, but they were relatively distinct from other common dimensions of childhood behavioral dysfunction. Twin correlations for the full range of scores and concordance rates for the extremes suggested moderate genetic influences, with some indication that the tactile domain might be more heritable than the auditory domain. C1 Univ Wisconsin, Dept Psychol, Waisman Ctr, Madison, WI 53706 USA. 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PD JUN PY 2006 VL 34 IS 3 BP 393 EP 407 DI 10.1007/s10802-006-9024-0 PG 15 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 057ZD UT WOS:000238632800009 PM 16649001 ER PT J AU Petscher, ES Bailey, JS AF Petscher, ES Bailey, JS TI Effects of training, prompting, and self-monitoring on staff behavior in a classroom for students with disabilities SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article; Proceedings Paper CT 25th Annual Meeting of the Florida-Association-of-Behavior-Analysis CY SEP, 2005 CL Sarasota, FL SP Florida Assoc Behav Anal DE staff training; self-monitoring; tactile prompt; classroom management ID TACTILE PROMPT; AUTISM; INITIATIONS; CHILDREN AB This study extended the limited research on the utility of tactile prompts and examined the effects of a treatment package on implementation of a token economy by instructional assistants in a classroom for students with disabilities. During baseline, we measured how accurately the assistants implemented a classroom token economy based on the routine training they had received through the school system. Baseline was followed by brief in-service training, which resulted in no improvement of token-economy implementation for recently hired instructional assistants. A treatment package of prompting and self-monitoring with accuracy feedback was then introduced as a multiple baseline design across behaviors. The treatment package was successfully faded to a more manageable self-monitoring intervention. Results showed visually significant improvements for all participants during observation sessions. C1 Florida State Univ, Dept Psychol, Tallahassee, FL 32306 USA. RP Petscher, ES (reprint author), Florida State Univ, Dept Psychol, Tallahassee, FL 32306 USA. EM Seligson@psy.fsu.edu CR Bailey J. S., 2002, RES METHODS APPL BEH BURGION LD, 1990, J APPL BEHAV ANAL, V23, P111, DOI 10.1901/jaba.1990.23-111 GABLE RA, 1999, ADDRESSING STUDENT 2 HARRIS KR, 1986, J APPL BEHAV ANAL, V19, P417, DOI 10.1901/jaba.1986.19-417 RICHMAN GS, 1988, J APPL BEHAV ANAL, V21, P401, DOI 10.1901/jaba.1988.21-401 Shabani DB, 2002, J APPL BEHAV ANAL, V35, P79, DOI 10.1901/jaba.2002.35-79 Taylor BA, 1998, J APPL BEHAV ANAL, V31, P651, DOI 10.1901/jaba.1998.31-651 Taylor BA, 2004, J APPL BEHAV ANAL, V37, P79, DOI 10.1901/jaba.2004.37-79 NR 8 TC 10 Z9 10 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2006 VL 39 IS 2 BP 215 EP 226 DI 10.1901/jaba.2006.02-05 PG 12 WC Psychology, Clinical SC Psychology GA 049EC UT WOS:000237997700006 PM 16813042 ER PT J AU Lerman, DC Addison, LR Kodak, T AF Lerman, Dorothea C. Addison, Laura R. Kodak, Tiffany TI A preliminary analysis of self-control with aversive events: The effects of task magnitude and delay on the choices of children with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE aversive events; self-control; task magnitude; task delay ID BEHAVIOR; ESCAPE AB When faced with a choice between two aversive events, a person exhibits self-control by choosing a smaller, more immediate aversive event over a larger, delayed aversive event. Task demands are often aversive to children with autism and other developmental disabilities. The purpose of this study was to evaluate behavioral sensitivity to differences in the amount and delay of tasks as part of a preliminary study on self-control. Participants were 2 children with autism who engaged in problem behavior maintained by escape. Results indicated a lack of self-control with respect to choosing between two aversive tasks and suggested potential strategies for increasing self-control (i.e., choosing a small immediate task over a large delayed task). C1 Univ Houston Clear Lake, Houston, TX 77058 USA. Louisiana State Univ, Baton Rouge, LA 70803 USA. RP Lerman, DC (reprint author), Univ Houston Clear Lake, 2700 Bay Area Blvd,Campus Box 245, Houston, TX 77058 USA. EM lerman@uhcl.edu CR DELUTY MZ, 1978, J EXP PSYCHOL ANIM B, V4, P250, DOI 10.1037//0097-7403.4.3.250 GRUSEC JE, 1968, J PERS SOC PSYCHOL, V9, P85, DOI 10.1037/h0025699 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P215, DOI 10.1901/jaba.1994.27-215 IWATA BA, 1990, J APPL BEHAV ANAL, V23, P11, DOI 10.1901/jaba.1990.23-11 Romaniuk C, 2002, J APPL BEHAV ANAL, V35, P349, DOI 10.1901/jaba.2002.35-349 NR 5 TC 6 Z9 6 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2006 VL 39 IS 2 BP 227 EP 232 DI 10.1901/jaba.2006.90-05 PG 6 WC Psychology, Clinical SC Psychology GA 049EC UT WOS:000237997700007 PM 16813043 ER PT J AU Williams, G Carnerero, JJ Perez-Gonzalez, LA AF Williams, G Carnerero, JJ Perez-Gonzalez, LA TI Generalization of tacting actions in children with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE tacts; labeling; generalization; tacting actions; spontaneous language; autism AB This intervention compared the effects of two procedures on the generalization of a tacting repertoire (labeling) in 6 children with autism spectrum disorder. In one procedure the verbal antecedent stimulus "What is she doing?" appeared together with a person performing an action; in the other procedure, the antecedent stimulus was just the presence of the action. In initial tests, children emitted tacts only when the action was presented with the verbal antecedent. Thereafter, they learned to tact an action without the verbal antecedent and received tests to evaluate generalization to another action. Results indicated that in order to obtain generalization of tacting actions, it was necessary to learn to tact other actions without the verbal antecedent as well as learning to tact the action with the verbal antecedent. These findings have relevance for generalization of tacting actions from control by verbal antecedents to natural conditions and the production of spontaneous language. C1 Ctr Mudaris, Cordoba, Spain. Univ Oviedo, Oviedo, Spain. RP Williams, G (reprint author), Appl Behav Consultant Serv Inc, 66 Regency Circle, Englewood, NJ 07631 USA. EM gladyswilliams2003@hotmail.com; laperez@uniovi.es RI Perez-Gonzalez, Luis/L-2338-2014 CR GREER RD, 1986, PILOT VERSION SCRIPT GUESS D, 1976, FUNCTIONAL SPEECH LA Krantz PJ, 1998, J APPL BEHAV ANAL, V31, P191, DOI 10.1901/jaba.1998.31-191 PARTINGTON JW, 1994, J APPL BEHAV ANAL, V27, P733, DOI 10.1901/jaba.1994.27-733 Sundberg M L, 2000, Anal Verbal Behav, V17, P89 Williams G., 1993, BEHAVIOROLOGY, V1, P31 NR 6 TC 7 Z9 7 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2006 VL 39 IS 2 BP 233 EP 237 DI 10.1901/jaba.2006.175-04 PG 5 WC Psychology, Clinical SC Psychology GA 049EC UT WOS:000237997700008 PM 16813044 ER PT J AU O'Reilly, MF Sigafoos, J Edrisinha, C Lancioni, G Cannella, H Choi, HY Barretto, A AF O'Reilly, MF Sigafoos, J Edrisinha, C Lancioni, G Cannella, H Choi, HY Barretto, A TI A preliminary examination of the evocative effects of the establishing operation SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; establishing operations; extinction; functional analysis; antecedent assessment ID REFINEMENTS AB We attempted to isolate the evocative effects of the establishing operation for positively reinforced problem behavior with 2 participants. The study consisted of three phases. First, a functional analysis identified tangible items (Participant 1) and attention (Participant 2) as maintaining problem behavior. Second, access to tangible items and attention was systematically controlled (continuous access vs. no access) immediately prior to functional analysis sessions in which these consequences were delivered contingent on problem behavior. Results of this phase indicated that problem behavior occurred at higher levels when access to tangible items and attention was restricted. In the third phase, prior access was again controlled, but problem behavior produced no consequences. Results of this final phase indicated that problem behavior occurred at higher levels during extinction sessions when participants did not have prior access to the reinforcers. C1 Univ Texas, Dept Special Educ, Austin, TX 78712 USA. Univ Tasmania, Hobart, Tas 7001, Australia. Univ Bari, Bari, Italy. Gonzaga Univ, Spokane, WA 99258 USA. RP O'Reilly, MF (reprint author), Univ Texas, Dept Special Educ, 1 Univ Stn D5300, Austin, TX 78712 USA. EM markoreilly@mail.utexas.edu CR IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Laraway S, 2003, J APPL BEHAV ANAL, V36, P407, DOI 10.1901/jaba.2003.36-407 Lerman DC, 1996, J APPL BEHAV ANAL, V29, P345, DOI 10.1901/jaba.1996.29-345 Michael J, 2000, J APPL BEHAV ANAL, V33, P401, DOI 10.1901/jaba.2000.33-401 MICHAEL J, 1982, J EXP ANAL BEHAV, V37, P149, DOI 10.1901/jeab.1982.37-149 MICHAEL J, 1993, BEHAV ANALYST, V16, P191 Schopler E., 1988, CHILDHOOD AUTISM RAT Sparrow S, 1984, VINELAND ADAPTIVE BE VOLLMER TR, 1991, J APPL BEHAV ANAL, V24, P279, DOI 10.1901/jaba.1991.24-279 NR 9 TC 18 Z9 18 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2006 VL 39 IS 2 BP 239 EP 242 DI 10.1901/jaba.2006.160-04 PG 4 WC Psychology, Clinical SC Psychology GA 049EC UT WOS:000237997700009 PM 16813045 ER PT J AU Sokol, DK Chen, DM Farlow, MR Dunn, DW Maloney, B Zimmer, JA Lahiri, DK AF Sokol, Deborah K. Chen, Demao Farlow, Martin R. Dunn, David W. Maloney, Bryan Zimmer, Jennifer A. Lahiri, Debomoy K. TI High levels of Alzheimer beta-amyloid precursor protein (APP) in children with severely autistic behavior and aggression SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID MAGNETIC-RESONANCE SPECTROSCOPY; DISEASE; RECEPTOR; BRAIN; GENE; PEPTIDES; DISORDER; CORTEX AB Autism is characterized by restricted, repetitive behaviors and impairment in socialization and communication. Although no neuropathologic substrate underlying autism has been found, the findings of brain overgrowth via neuroimaging studies and increased levels of brain-derived neurotrophic factor (BDNF) in neuropathologic and blood studies favor an anabolic state. We examined acety1cholinesterase, plasma neuronal proteins, secreted beta-amyloid precursor protein (APP), and amyloid-beta 40 and amyloid-beta 42 peptides in children with and without autism. Children with severe autism and aggression expressed secreted beta-amyloid precursor protein at two or more times the levels of children without autism and up to four times more than children with mild autism. There was a trend for children with autism to show higher levels of secreted beta-amyloid precursor protein and nonamyloidogenic secreted beta-amyloid precursor protein and lower levels of amyloid-beta 40 compared with controls. This favors an increased (x-secretase pathway in autism (anabolic), opposite to what is seen in Alzheimer disease. Additionally, a complex relationship between age, acety1cholinesterase, and plasma neuronal markers was found. C1 Indiana Univ, Sch Med, Dept Neurol, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. RP Sokol, DK (reprint author), Indiana Univ, Riley Hosp Children, Sch Med, Pediat Neurol RI 1757, 702 Barnhill Dr, Indianapolis, IN 46202 USA. 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Child Neurol. PD JUN PY 2006 VL 21 IS 6 BP 444 EP 449 DI 10.2310/7010.2006.00130 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 069SW UT WOS:000239469500002 PM 16948926 ER PT J AU Nagaraj, R Singhi, P Malhi, P AF Nagaraj, Ravishankar Singhi, Pratibha Malhi, Prahbhjot TI Risperidone in children with autism: Randomized, placebo-controlled, double-blind study SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID RATING-SCALE; OPEN TRIAL; ADOLESCENTS; HALOPERIDOL AB Some open-label studies suggest that risperidone can be useful in the treatment of certain target symptoms in children with autism. We aimed to study whether the use of risperidone in comparison with placebo improved functioning in children with autism with regard to behavior (aggressiveness, hyperactivity, irritability), social and emotional responsiveness, and communication skills. We conducted a randomized, double-blind, placebo-controlled trial with 40 consecutive children with autism, whose ages ranged from 2 to 9 years, who were receiving either risperidone or placebo given orally at a dose of 1 mg/day for 6 months. Autism symptoms were monitored periodically. The outcome variables were total scores on the Childhood Autism Rating Scale (CARS) and the Children's Global Assessment Scale (CGAS) after 6 months. Of the 40 children enrolled, 39 completed the trial over a period of 18 months; 19 received risperidone, and 20 received placebo. In the risperidone group, 12 of 19 children showed improvement in the total Childhood Autism Rating Scale score and 17 of 19 children in the Children's Global Assessment Scale score compared with 0 of 20 children for the Childhood Autism Rating Scale,score and 2 of 20 children for the Children's Global Assessment Scale score in the placebo group (P <.001 and P =.035, respectively). Risperidone also improved social responsiveness and nonverbal communication and reduced the symptoms of hyperactivity and aggression. Risperidone was associated with increased appetite and a mild weight gain, mild sedation in 20%, and transient dyskinesias in three children. Risperidone improved global functioning and social responsiveness while reducing hyperactivity and aggression in children with autism and was well tolerated. C1 Postgrad Inst Med Educ & Res, Adv Pediat Ctr, Dept Pediat, Chandigarh 160012, India. RP Singhi, P (reprint author), Postgrad Inst Med Educ & Res, Adv Pediat Ctr, Dept Pediat, Sector 12, Chandigarh 160012, India. EM drsinghi@glide.net.in CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERSON LT, 1984, AM J PSYCHIAT, V141, P1195 Campbell M, 1997, J AM ACAD CHILD PSY, V36, P835, DOI 10.1097/00004583-199706000-00022 Campbell M, 1996, J AM ACAD CHILD PSY, V35, P134, DOI 10.1097/00004583-199602000-00005 CHOUINARD G, 1993, J CLIN PSYCHOPHARM, V13, P25 DILALLA DL, 1994, J AUTISM DEV DISORD, V24, P115, DOI 10.1007/BF02172092 Doll E A, 1965, Cereb Palsy J, V26, P3 *JANSS RES FDN, 1992, RISP TREATM CHRON SC JANSSEN PAJ, 1988, J PHARMACOL EXP THER, V244, P685 Malone RP, 2002, J AM ACAD CHILD PSY, V41, P140, DOI 10.1097/00004583-200202000-00007 Masi G, 2001, J AM ACAD CHILD PSY, V40, P1206, DOI 10.1097/00004583-200110000-00015 McDougle CJ, 1997, J AM ACAD CHILD PSY, V36, P685, DOI 10.1097/00004583-199705000-00020 MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 National Institute of Mental Health Alcohol Drug Abuse and Mental Health Administration Public Health Service Department of Health Education and Welfare, 1988, PSYCHOPHARMACOL B, V24, P781 Nicolson R, 1998, J AM ACAD CHILD PSY, V37, P372, DOI 10.1097/00004583-199804000-00014 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Santosh Paramala Janardhanan, 2001, Indian Journal of Pediatrics, V68, P427, DOI 10.1007/BF02723022 Schopler E., 1988, CHILDHOOD AUTISM RAT SHAFFER D, 1983, ARCH GEN PSYCHIAT, V40, P1228 NR 19 TC 65 Z9 70 PU B C DECKER INC PI HAMILTON PA 50 KING STREET EAST, 2ND FLOOR, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD JUN PY 2006 VL 21 IS 6 BP 450 EP 455 DI 10.2310/7010.2006.00099 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 069SW UT WOS:000239469500003 PM 16948927 ER PT J AU Carcani-Rathwell, I Rabe-Hesketh, S Santosh, PJ AF Carcani-Rathwell, Iris Rabe-Hesketh, Sophia Santosh, Paramala J. TI Repetitive and stereotyped behaviours in pervasive developmental disorders SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE repetitive and stereotyped behaviours; sensory and motor stereotypies; cognitive rigidity; pervasive developmental disorders; autism; mental retardation ID OBSESSIVE-COMPULSIVE DISORDER; MENTAL-RETARDATION; AUTISTIC-CHILDREN; PREVALENCE; PREDICTORS; INFANTS; HISTORY; TRAITS; TWIN AB Background: Repetitive and stereotyped behaviours are a heterogeneous group of behaviours present in many neuropsychiatric disorders. Despite their core significance in PDD, it is not clear whether there are distinct groups of these behaviours with different specificity to autism. Methods: A two-factor model of the repetitive behaviours, namely sensory/motor (lower-order) and cognitive rigidity (higher-order), was conceptualised. The model's goodness of fit to the data was examined in a clinic population of children with PDD, with and without mental retardation, and of those with only mental retardation (MR). Results: Subjects with PDD had higher rates of all repetitive behaviours compared to those with MR only. The existence of two independent 'lower-order' and 'higher-order' sub-groups of the repetitive behaviours was confirmed only in the MR group. The lower-order behaviours appear to be associated more with global developmental problems, whereas the higher-order behaviours were significantly associated with ruminations in the PDD group. Conclusions: This study suggests that there may be two distinct sub-groups of repetitive behaviours whereby the sensory and motor repetitive behaviours are generally associated with lower developmental age and less specific to the autistic syndrome whereas the 'higher-order' behaviours may be a more 'autism-specific' feature. The co-occurrence of the lower- and higher-order behaviours in PDD might reflect the end result of diffuse altered neural networks in these disorders thus being a specific feature of PDD. There is a need for more systematic studies of these behaviours not only in autistic disorders but also in other neuropsychiatric disorders. C1 S London & Maudsley NHS Trust, Child & Adolescent Psychiat, London, England. Univ Calif Berkeley, Grad Sch Educ, Berkeley, CA 94720 USA. Great Ormond St Hosp Sick Children, London WC1N 3JH, England. RP Carcani-Rathwell, I (reprint author), Kings Coll Hosp London, Belgrave Dept, Denmark Hill, London SE5 9RS, England. EM iris.carcani-rathwell@slam.nhs.uk RI Rabe-Hesketh, Sophia/B-1643-2008 OI Rabe-Hesketh, Sophia/0000-0002-5257-4837 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARTHUR G, 1952, ARTHUR ADAPTATION LE BACHARA GH, 1980, PERCEPT MOTOR SKILL, V50, P933 BAILEY A, 1995, PSYCHOL MED, V25, P63 Bejerot S, 2001, NORD J PSYCHIAT, V55, P169 Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x CAMPBELL M, 1990, PSYCHOPHARMACOL BULL, V26, P260 Cannon M, 2001, BRIT J PSYCHIAT, V178, P420, DOI 10.1192/bjp.178.5.420 CLARK P, 1981, J AUTISM DEV DISORD, V11, P201, DOI 10.1007/BF01531685 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 DADDS M, 1988, J CHILD PSYCHOL PSYC, V29, P669, DOI 10.1111/j.1469-7610.1988.tb01887.x Dunn L M., 1982, BRIT PICTURE VOCABUL Evans DW, 1997, CHILD DEV, V68, P58, DOI 10.2307/1131925 Frith U., 1989, AUTISM EXPLAINING EN FRITH UD, 1990, NEUROBIOLOGY STEREOT, P232 GOODMAN R, 1991, J CHILD PSYCHOL PSYC, V32, P551, DOI 10.1111/j.1469-7610.1991.tb00331.x Gross-Isseroff R, 2001, World J Biol Psychiatry, V2, P193 Hollander E, 2003, PSYCHIAT RES, V117, P11, DOI 10.1016/S0165-1781(02)00304-9 Kanner L, 1943, NERV CHILD, V2, P217 Kerr A M, 2001, Pediatr Rehabil, V4, P157, DOI 10.1080/13638490210121694 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MCDOUGLE CJ, 1995, AM J PSYCHIAT, V152, P772 Militerni R, 2002, EUR CHILD ADOLES PSY, V11, P210, DOI 10.1007/s00787-002-0279-x Osterling JA, 2002, DEV PSYCHOPATHOL, V14, P239 Pierce K, 2001, BIOL PSYCHIAT, V49, P655, DOI 10.1016/S0006-3223(00)01008-8 Rabe-Hesketh S, 2004, PSYCHOMETRIKA, V69, P167, DOI 10.1007/BF02295939 Rabe-Hesketh S, 2002, STATA J, V2, P1 Raven J. C., 1956, GUIDE USING COLOURED RUNCO MA, 1986, J AUTISM DEV DISORD, V16, P31, DOI 10.1007/BF01531576 SANTOSH P, IN PRESS EUROPEAN J Simic M, 2001, J AFFECT DISORDERS, V62, P175, DOI 10.1016/S0165-0327(99)00201-3 SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 Szatmari P, 2003, J CHILD PSYCHOL PSYC, V44, P520, DOI 10.1111/1469-7610.00141 THELEN E, 1981, ANIM BEHAV, V2, P3 TROSTER H, 1991, J ABNORM CHILD PSYCH, V19, P569, DOI 10.1007/BF00925821 Turner M, 1999, J CHILD PSYCHOL PSYC, V40, P839, DOI 10.1017/S0021963099004278 Turner M. A., 1997, AUTISM EXECUTIVE DIS, P57 VOLKMAR FR, 1995, J AM ACAD CHILD PSY, V34, P1092, DOI 10.1097/00004583-199508000-00020 Wechsler D., 1974, MANUAL WECHSLER INTE Willemsen-Swinkels SHN, 1998, J AUTISM DEV DISORD, V28, P547, DOI 10.1023/A:1026008313284 World Health Organization, 1992, 10 REV INT CLASS DIS NR 43 TC 55 Z9 55 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD JUN PY 2006 VL 47 IS 6 BP 573 EP 581 DI 10.1111/j.1469-7610.2005.01565.x PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 043XT UT WOS:000237636900006 PM 16712634 ER PT J AU Szatmari, P Georgiades, S Bryson, S Zwaigenbaum, L Roberts, W Mahoney, W Goldberg, J Tuff, L AF Szatmari, P Georgiades, S Bryson, S Zwaigenbaum, L Roberts, W Mahoney, W Goldberg, J Tuff, L TI Investigating the structure of the restricted, repetitive behaviours and interests domain of autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE pervasive developmental disorders; autism; restricted repetitive behaviours and interests; principal components analysis; structure of autism domains; genetic studies ID DIAGNOSTIC OBSERVATION SCHEDULE; SPECTRUM DISORDER; INTERVIEW; SUBTYPES AB Background: The Restricted, Repetitive Behaviours and Interests (RRBIs) are represented in the DSM-IV and measured by the Autism Diagnostic Interview-Revised (ADI-R) as one of the three homogeneous symptom categories of Pervasive Developmental Disorders. Although this conceptualisation is well accepted in the field, the grouping of symptoms is based primarily on clinical judgment rather than on empirical evidence. Methods: The objective of this study was to examine the factor structure of the RRBI domain of autism. Eleven items from this domain of the ADI-R were used in a Principal Components Analysis (PCA). Our sample consisted of 339 individuals with a Best Estimate diagnosis of Pervasive Developmental Disorder (PDD). Results: Findings indicate that the RRBI domain is composed of two distinct factors or dimensions: Insistence on Sameness ( IS) and Repetitive Sensory and Motor Behaviours (RSMB). RSMB is negatively correlated with adaptive skills; that is, lower functioning individuals tend to have higher levels of repetitive sensory and motor behaviours. On the other hand, IS is positively correlated with autistic symptoms in the communication and language domain. Further analyses suggest moderate familial aggregation among affected sibling pairs within the IS but not the RSMB factor. Conclusions: These results provide evidence for the heterogeneity of the RRBI domain of the ADI-R in terms of both clinical presentation and other correlates. In addition, the IS factor seems to be under familial (presumably genetic) control, while RSMB appears to simply reflect variation in developmental level. C1 McMaster Univ, Offord Ctr Child Studies, Dept Psychiat & Behav Neurosci, Hamilton, ON L8N 3Z5, Canada. McMaster Univ, Dept Pediat, Hamilton, ON L8N 3Z5, Canada. Dalhousie Univ, IWK Hlth Ctr, Dept Pediat, Halifax, NS B3H 3J5, Canada. Dalhousie Univ, IWK Hlth Ctr, Dept Psychol, Halifax, NS B3H 3J5, Canada. Univ Toronto, Hosp Sick Children, Dept Pediat, Toronto, ON M5G 1X8, Canada. RP Szatmari, P (reprint author), McMaster Univ, Offord Ctr Child Studies, Dept Psychiat & Behav Neurosci, Chedoke Site,Patterson Bldg,1200 Main St W, Hamilton, ON L8N 3Z5, Canada. EM szatmar@mcmaster.ca CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARMITAGE P, 1998, ENCY BIOSTATISTICS, V5 Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 Cuccaro ML, 2003, CHILD PSYCHIAT HUM D, V34, P3, DOI 10.1023/A:1025321707947 Dunteman G. 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Child Psychol. Psychiatry PD JUN PY 2006 VL 47 IS 6 BP 582 EP 590 DI 10.1111/j.1469-7610.2005.01537.x PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 043XT UT WOS:000237636900007 PM 16712635 ER PT J AU Baranek, GT David, FJ Poe, MD Stone, WL Watson, LR AF Baranek, GT David, FJ Poe, MD Stone, WL Watson, LR TI Sensory Experiences Questionnaire: discriminating sensory features in young children with autism, developmental delays, and typical development SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE sensory modulation/processing; hyper/hyporesponsiveness; autism; developmental disabilities ID DISORDERS; ATTENTION; PROFILE; MODEL; DISABILITIES; INTEGRATION; INTERVIEW; RESPONSES; SYMPTOMS; MOTOR AB Background: This study describes a new caregiver-report assessment, the Sensory Experiences Questionnaire (SEQ), and explicates the nature of sensory patterns of hyper- and hyporesponsiveness, their prevalence, and developmental correlates in autism relative to comparison groups. Method: Caregivers of 258 children in five diagnostic groups (Autism, PDD, DD/MR, Other DD, Typical) ages 5 - 80 months completed the SEQ. Results: The SEQ's internal consistency was alpha = .80. Prevalence of overall sensory symptoms for the Autism group was 69%. Sensory symptoms were inversely related to mental age. The Autism group had significantly higher symptoms than either the Typical or DD groups and presented with a unique pattern of response to sensory stimuli-hyporesponsiveness in both social and nonsocial contexts. A pattern of hyperresponsiveness was similar in the Autism and DD groups, but significantly greater in both clinical groups than in the Typical group. Conclusion: The SEQ was able to characterize sensory features in young children with autism, and differentiate their sensory patterns from comparison groups. These unique sensory patterns have etiological implications, as well as relevance for assessment and intervention practices. 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Psychiatry PD JUN PY 2006 VL 47 IS 6 BP 591 EP 601 DI 10.1111/j.1469-7610.2005.01546.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 043XT UT WOS:000237636900008 PM 16712636 ER PT J AU Hessl, D Glaser, B Dyer-Friedman, J Reiss, AL AF Hessl, D Glaser, B Dyer-Friedman, J Reiss, AL TI Social behavior and cortisol reactivity in children with fragile X syndrome SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE fragile X syndrome; cortisol; anxiety; social phobia; FMR1 gene; gaze; autism ID SALIVARY CORTISOL; PRECOCIOUS PUBERTY; MALES; DISORDERS; CHECKLIST; PHOBIA AB Objective: To examine the association between limbic-hypothalamic-pituitary-adrenal (L-HPA) axis reactivity and social behavior in children with fragile X syndrome (FXS). Method: Salivary cortisol changes and concurrent anxiety-related behaviors consistent with the behavioral phenotype of FXS were measured in 90 children with the fragile X full mutation and their 90 unaffected siblings during a social challenge task in the home. Results: Boys and girls with FXS demonstrated more gaze aversion, task avoidance, behavioral signs of distress, and poorer vocal quality than the unaffected siblings. Multiple regression analyses showed that after accounting for effects of IQ, gender, age, quality of the home environment, and basal cortisol level, cortisol reactivity to the task was significantly associated with social gaze in children with FXS. The most gaze-aversive children with FXS had cortisol reductions, whereas those with more eye contact demonstrated the most cortisol reactivity. Unaffected siblings demonstrated an opposite pattern in which less eye contact was associated with increased cortisol reactivity. Conclusions: Results of the study suggest a unique relation between abnormal gaze behavior and L-HPA mediated stress reactivity in FXS. C1 Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. Univ Calif Davis, Dept Psychiat & Behav Sci, Davis, CA 95616 USA. Univ Denver, Dept Psychol, Denver, CO 80208 USA. Stanford Univ, Dept Psychiat, Div Child & Adolescent Psychiat, Stanford, CA 94305 USA. RP Reiss, AL (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, 401 Quarry Rd, Stanford, CA 94305 USA. EM reiss@stanford.edu CR ACHENBACH TM, 1991, MANUAL CHILD BEAHV C AMAN MG, 1985, AM J MENT DEF, V89, P485 Belser RC, 1995, DEV BRAIN DYSFUNCT, V8, P270 BREGMAN JD, 1990, YALE J BIOL MED, V63, P293 BREGMAN JD, 1988, J AUTISM DEV DISORD, V18, P343, DOI 10.1007/BF02212191 BUTLER MG, 1988, AM J MED GENET, V31, P779, DOI 10.1002/ajmg.1320310408 Caldwell B. M., 1984, HOME OBSERVATION MEA COHEN IL, 1988, AM J MENT RETARD, V92, P436 Derogatis L. 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Child Psychol. Psychiatry PD JUN PY 2006 VL 47 IS 6 BP 602 EP 610 DI 10.1111/j.1469-7610.2005.01556.x PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 043XT UT WOS:000237636900009 PM 16712637 ER PT J AU Kasari, C Freeman, S Paparella, T AF Kasari, C Freeman, S Paparella, T TI Joint attention and symbolic play in young children with autism: a randomized controlled intervention study SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE intervention; joint attention; symbolic play; autism ID BEHAVIORAL TREATMENT; PRESCHOOL-CHILDREN; LANGUAGE; SKILLS; DEFICITS AB Background: Delays and deficits in joint attention and symbolic play constitute two important developmental problems in young children with autism. These areas of deficit have been well studied in autism but have rarely been the focus of treatment efforts (see Kasari, Freeman, & Paparella, 2001). In this study, we examine the efficacy of targeted interventions of joint attention and symbolic play. Methods: Participants were 58 children with autism aged 3 and 4 years ( 46 boys). Children were randomized to a joint attention intervention, a symbolic play intervention, or control group. Interventions were conducted 30 minutes daily for 5 - 6 weeks. Both structured assessments of joint attention and play skills and mother - child interactions were collected pre and post intervention by independent assessors. Results: Results indicate that both intervention groups improved significantly over the control group on certain behaviors. Children in the joint attention intervention initiated significantly more showing and responsiveness to joint attention on the structured joint attention assessment and more child-initiated joint attention in the mother - child interaction. The children in the play group showed more diverse types of symbolic play in interaction with their mothers and higher play levels on both the play assessment and in interaction with their mothers. Conclusions: This randomized controlled trial provides promising data on the specificity and generalizability of joint attention and play interventions for young children with autism. Future studies need to examine the long-term effects of these early interventions on children's development. C1 Univ Calif Los Angeles, Los Angeles, CA 90095 USA. RP Kasari, C (reprint author), Univ Calif Los Angeles, 3132 Moore Hall, Los Angeles, CA 90095 USA. EM Kasari@gseis.ucla.edu CR BAKEMAN R, 1984, CHILD DEV, V55, P1278, DOI 10.2307/1129997 Baron-Cohen S., 1994, UNDERSTANDING OTHER BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Baron-Cohen S, 1997, HDB AUTISM PERVASIVE, P880 Chambless DL, 1998, J CONSULT CLIN PSYCH, V66, P7, DOI 10.1037//0022-006X.66.1.7 Charman T, 2003, INT J LANG COMM DIS, V38, P265, DOI 10.1080/136820310000104830 Drew A, 2002, EUR CHILD ADOLES PSY, V11, P266, DOI 10.1007/s00787-002-0299-6 TOMASELLO M, 1986, CHILD DEV, V57, P1454, DOI 10.1111/j.1467-8624.1986.tb00470.x Gresham FM, 1998, J AUTISM DEV DISORD, V28, P5, DOI 10.1023/A:1026002717402 Hobson P, 2002, CRADLE THOUGHT EXPLO Hwang B, 2000, J AUTISM DEV DISORD, V30, P331, DOI 10.1023/A:1005579317085 Kasari C, 2001, INT REV RES MENT RET, V23, P207 Kasari C, 2002, J AUTISM DEV DISORD, V32, P447, DOI 10.1023/A:1020546006971 Koegel RL, 1999, SCHOOL PSYCHOL REV, V28, P576 LEWY AL, 1992, J ABNORM CHILD PSYCH, V20, P555, DOI 10.1007/BF00911240 Lonigan CJ, 1998, J CLIN CHILD PSYCHOL, V27, P138, DOI 10.1207/s15374424jccp2702_1 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 LORD C, 1993, INF MENTAL HLTH J, V14, P234, DOI 10.1002/1097-0355(199323)14:3<234::AID-IMHJ2280140308>3.0.CO;2-F LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 LOVELAND KA, 1986, J AUTISM DEV DISORD, V16, P335, DOI 10.1007/BF01531663 MUNDY P, 1994, DEV PSYCHOPATHOL, V6, P389, DOI 10.1017/S0954579400006003 MUNDY P, 1986, J CHILD PSYCHOL PSYC, V27, P657, DOI 10.1111/j.1469-7610.1986.tb00190.x MUNDY P, 1990, J AUTISM DEV DISORD, V20, P115, DOI 10.1007/BF02206861 Mundy P, 1996, PRELIMINARY MANUAL, pA preliminary National Research Council, 2001, ED CHILDR AUT NINIO A, 1978, J CHILD LANG, V5, P1 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Roeyers H, 1998, DEV PSYCHOPATHOL, V10, P441, DOI 10.1017/S0954579498001680 ROGERS SJ, 1989, J AM ACAD CHILD PSY, V28, P207, DOI 10.1097/00004583-198903000-00010 Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 Sigman M., 1999, MONOGRAPHS SOC RES C, V64 SIGMAN M, 1984, DEV PSYCHOL, V20, P293, DOI 10.1037/0012-1649.20.2.293 STAHMER AC, 1995, J AUTISM DEV DISORD, V25, P123, DOI 10.1007/BF02178500 UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 WARREN SF, 1986, J SPEECH HEAR DISORD, V51, P239 Weiss Robert E., 2005, MODELING LONGITUDINA Whalen C, 2003, J CHILD PSYCHOL PSYC, V44, P456, DOI 10.1111/1469-7610.00135 Witte JS, 2000, EPIDEMIOLOGY, V11, P684, DOI 10.1097/00001648-200011000-00012 Wolery M, 2002, J AUTISM DEV DISORD, V32, P463, DOI 10.1023/A:1020598023809 NR 39 TC 184 Z9 188 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD JUN PY 2006 VL 47 IS 6 BP 611 EP 620 DI 10.1111/j.1469-7610.2005.01567.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 043XT UT WOS:000237636900010 PM 16712638 ER PT J AU Conti-Ramsden, G Simkin, Z Botting, N AF Conti-Ramsden, Gina Simkin, Zoe Botting, Nicola TI The prevalence of autistic spectrum disorders in adolescents with a history of specific language impairment (SLI) SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE specific language impairment (SLI); autism; prevalence; diagnosis ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; CHILDREN; AGE; UPDATE AB Background: Traditionally, autism and specific language impairment (SLI) have been regarded as distinct disorders but, more recently, evidence has been put forward for a closer link between them: a common set of language problems, in particular receptive language difficulties and the existence of intermediate cases including pragmatic language impairment. The present study aimed to examine the prevalence of autism spectrum disorders in a large sample of adolescents with a history of SLI. Method: The presence of autism spectrum disorders was examined in seventy-six 14-year-olds with a confirmed history of SLI. A variety of instruments were employed, including the Autism Diagnostic Interview-Revised (ADI-R), the Autism Diagnostic Observation Schedule (ADOS) and the Family History Interview (FHI). Results: The prevalence of autism spectrum disorders in young people with SLI was found to be 3.9%, about 10 times what would be expected from the general population. In addition, a much larger number of young people with a history of SLI showed only some autism spectrum symptoms or showed them in a mild form. Conclusions: Young people with SLI have an increased risk of autism. The magnitude of this risk is considerable. In addition, a larger proportion ( a quarter of individuals) present with a number of behaviours consistent with autism spectrum disorders. C1 Univ Manchester, Sch Psychol Sci, Manchester M13 9PL, Lancs, England. RP Conti-Ramsden, G (reprint author), Univ Manchester, Sch Psychol Sci, Devas St Bldg,Oxford Rd, Manchester M13 9PL, Lancs, England. EM gina.conti-ramsden@manchester.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4 Bishop D. V. M., 2000, SPEECH LANGUAGE IMPA Bishop DVM, 2003, NOVART FDN SYMP, V251, P213 Bishop DVM, 2002, J CHILD PSYCHOL PSYC, V43, P917, DOI 10.1111/1469-7610.00114 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Botting N, 2005, J CHILD PSYCHOL PSYC, V46, P317, DOI 10.1111/j.1469-7610.2004.00355.x Botting N, 2003, DEV MED CHILD NEUROL, V45, P515 Charman T, 2002, EUR CHILD ADOLES PSY, V11, P249, DOI 10.1007/s00787-002-0297-8 Charman T, 2005, J CHILD PSYCHOL PSYC, V46, P500, DOI 10.1111/j.1469-7610.2004.00377.x Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Conti-Ramsden G, 1999, INT J LANG COMM DIS, V34, P359 ContiRamsden G, 1997, J SPEECH LANG HEAR R, V40, P765 Conti-Ramsden G., 1999, AUTISM, V3, P371, DOI 10.1177/1362361399003004005 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 GILLBERG C, 1990, J CHILD PSYCHOL PSYC, V31, P921, DOI 10.1111/j.1469-7610.1990.tb00834.x Hollander M, 1973, NONPARAMETRIC STAT M LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LEONARD LB, 1998, CHILDREN SPECIFIC LA Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Noterdaeme M, 2002, AUTISM, V6, P159, DOI 10.1177/1362361302006002003 Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 *PSYCH CORP, 1992, WECHSL INT SCAL CHIL Rapin I, 1998, INT J LANG COMM DIS, V33, P82 Rapin I, 1996, J CHILD PSYCHOL PSYC, V37, P643, DOI 10.1111/j.1469-7610.1996.tb01456.x Rust J, 1993, WECHSLER OBJECTIVE R Rutter M. A., 1967, J CHILD PSYCHOL PSYC, V9, P1 Semel E., 1987, CLIN EVALUATION LANG Tomblin JB, 1997, J SPEECH LANG HEAR R, V40, P1245 WHO, 1993, ICD 10 CLASS MENT BE Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 NR 33 TC 61 Z9 62 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD JUN PY 2006 VL 47 IS 6 BP 621 EP 628 DI 10.1111/j.1469-7610.2005.01584.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 043XT UT WOS:000237636900011 PM 16712639 ER PT J AU Landa, R Garrett-Mayer, E AF Landa, R Garrett-Mayer, E TI Development in infants with autism spectrum disorders: a prospective study SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; autism spectrum disorder; autistic disorder; language impairment; language delay; language disorder; motor skills; pervasive developmental disorder; siblings ID YOUNG-CHILDREN; MENTAL-RETARDATION; EARLY RECOGNITION; HOME VIDEOTAPES; FAMILY HISTORY; FOLLOW-UP; MOTOR; AGE; REGRESSION; IMITATION AB Background: Autism is rarely diagnosed before three years of age despite evidence suggesting prenatal abnormalities in neurobiological processes. Little is known about when or how development becomes disrupted in the first two years of life in autism. Such information is needed to facilitate early detection and early intervention. Methods: This prospective study of autism spectrum disorders (ASD) examined development using the Mullen Scales of Early Learning (MSEL) in 87 infants tested at target ages 6, 14, and 24 months. Participants came from infants at high risk (siblings of children with autism) and low risk (no family history of autism) groups. Based on language test scores, Autism Diagnostic Observation Schedule, and clinical judgment at 24 months of age, participants were categorized as: unaffected, ASD, or language delayed (LD). Longitudinal linear regression and ANOVA models were applied to MSEL raw scores, and estimates were compared between the three diagnostic groups. Results: No statistically significant group differences were detected at 6 months. By 14 months of age, the ASD group performed significantly worse than the unaffected group on all scales except Visual Reception. By 24 months of age, the ASD group performed significantly worse than the unaffected group in all domains, and worse than the language delayed group in Gross Motor, Fine Motor, and Receptive Language. The developmental trajectory of the ASD group was slower than the other groups', and showed a significant decrease in development between the first and second birthdays. Conclusions: Variations from typical and language delayed development are detectable in many children with ASD using a measure of general development by 24 months of age. Unusual slowing in performance occurred between 14 and 24 months of age in ASD. C1 Johns Hopkins Sch Med, Ctr Autism & Related Disorders, Kennedy Krieger Inst, Baltimore, MD 21211 USA. Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Div Biostat, Baltimore, MD 21218 USA. RP Landa, R (reprint author), Johns Hopkins Sch Med, Ctr Autism & Related Disorders, Kennedy Krieger Inst, 3901 Greenspring Ave, Baltimore, MD 21211 USA. 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Psychiatry PD JUN PY 2006 VL 47 IS 6 BP 629 EP 638 DI 10.1111/j.1469-7610.2006.01531.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 043XT UT WOS:000237636900012 PM 16712640 ER PT J AU Bolte, S Poustka, F AF Bolte, S Poustka, F TI The broader cognitive phenotype of autism in parents: how specific is the tendency for local processing and executive dysfunction? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; phenotype; executive function; local processing; genetics ID WEAK CENTRAL COHERENCE; 1ST-DEGREE RELATIVES; SUBCLINICAL MARKERS; ASPERGERS-SYNDROME; CHILDREN; SCHIZOPHRENIA; SIBLINGS; DEFICITS; METAANALYSIS; DISORDERS AB Background: The objective of this study was to investigate the tendency for local processing style ('weak central coherence') and executive dysfunction in parents of subjects with an autism spectrum disorder (ASD) compared with parents of individuals with early onset schizophrenia (EOS) and mental retardation (MR). Method: Sixty-two parents of subjects with ASD, 36 parents of subjects with EOS and 30 parents of subjects with MR were examined. Data on two scales indicative of local visual processing (Embedded Figures Test, Block Design) and on three executive function tests ( Wisconsin Card Sorting Test, Tower of Hanoi, Trailmaking Test) were collected for all participants. Results: Parents of subjects with ASD performed significantly faster on the Embedded Figures Test compared with both control samples. No other substantial group differences were observed. Conclusions: The findings indicate that an increased tendency for local processing in terms of visual disembedding could be a relatively specific core feature of the broader cognitive phenotype of autism in parents. C1 Univ Frankfurt, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Dept Child & Adolescent Psychiat, D-60528 Frankfurt, Germany. RP Bolte, S (reprint author), Univ Frankfurt, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Dept Child & Adolescent Psychiat, Deutschordenstr 50, D-60528 Frankfurt, Germany. 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TI Early categorization of animate/inanimate concepts in young children with autism SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; categorization; cognitive processes; cognitive development ID DYNAMIC FEATURES; INFANCY; PERCEPTION; KNOWLEDGE; IMITATION AB Categorization and concept formation deficits along with other cognitive processing deficits have been suggested in individuals with Autism Spectrum Disorders (ASD). A compelling early cognitive deficit is the formation of coherent concepts for animates and inanimates. Development of such concepts is thought to be a crucial building block for young children's emerging understanding that different object kinds possess different physical, psychological, biological, and motion-related properties [Rakison, D. H., and Poulin-Dubois, D. (2001). Psychol. Bull. 127(2): 209-228]. In this preliminary study, 11 preschoolers with ASD participated in two experiments that tested early concept formation. A visually-based habituation paradigm was used to test whether young children with ASD could detect correlations among static and dynamic cues and whether they were selective in the correlations to which they attend. A more interactive imitation task was used to test children's knowledge of simple linear and nonlinear motions of animates and inanimates. Results suggest that the preschoolers with autism are delayed in the processes by which they form categories but nonetheless possess relevant knowledge about the motion properties of animates and inanimates. Implications of this preliminary study are discussed. C1 Univ Pittsburgh, Sch Med, Childrens Hosp, Autism Ctr, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, Pittsburgh, PA 15213 USA. RP Johnson, CR (reprint author), Univ Pittsburgh, Sch Med, Childrens Hosp, Autism Ctr, 3705 5th Ave, Pittsburgh, PA 15213 USA. EM Cynthia.Johnson@chp.edu CR Baron-Cohen S., 1995, MIND BLINDNESS ESSAY Castelli F, 2002, BRAIN, V125, P1839, DOI 10.1093/brain/awf189 Dawson G., 1997, EFFECTIVENESS EARLY, P307 EIMAS PD, 1994, COGNITION, V50, P83, DOI 10.1016/0010-0277(94)90022-1 Grandin T., 1995, THINKING PICTURES JONES SS, 1993, COGNITIVE DEV, V8, P113, DOI 10.1016/0885-2014(93)90008-S Klinger LG, 2001, DEV PSYCHOPATHOL, V13, P111, DOI 10.1017/S0954579401001080 Leaf R., 1999, WORK PROGR BEHAV MAN Lord C., 1999, AUTISM DIAGNOSTIC OB Lovaas O. 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Dev. Phys. Disabil. PD JUN PY 2006 VL 18 IS 2 BP 73 EP 89 DI 10.1007/s10882-006-9007-7 PG 17 WC Rehabilitation SC Rehabilitation GA 102UW UT WOS:000241839800001 ER PT J AU Boggs, KM Gross, AM Gohm, CL AF Boggs, Koren M. Gross, Alan M. Gohm, Carol L. TI Validity of the Asperger syndrome Diagnostic Scale SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE Asperger syndrome; Asperger's disorder; diagnosis; external validity ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM; SPECTRUM AB Until publication of the Asperger Syndrome Diagnostic Scale (ASDS) in 2001, no standardized and nationally-normed instrument existed specifically for the purpose of diagnosing Asperger syndrome (AS) [Myles et al., 2001. Asperger Syndrome Diagnostic Scale ASDS), PRO-ED, Austin]. This study sought to augment the existing psychometric data on the ASDS through examination of its divergent, convergent, and discriminative validity. Measures of AS, autism, and social skills competence were administered to 76 children with AS, autism, intellectually gifted children, and a control group of typically developing children without AS or autism. Results supported the divergent and convergent validity of the ASDS. Discriminative validity was partially supported. The ASDS was the best discriminator between children with AS and those without AS. Diagnostic accuracy for those with AS and autism was enhanced when scores on the ASDS were combined with scores on the Gilliam Autism Rating Scale (GARS) and the Social Skills Rating System (SSRS). Findings are discussed relative to the debate over the external validity of AS and the resulting limitations on research in the area. C1 Univ Mississippi, Dept Psychol, University, MS 38677 USA. RP Gross, AM (reprint author), Univ Mississippi, Dept Psychol, Peabody Bldg, University, MS 38677 USA. EM pygross@olemiss.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Attwood T., 1998, ASPERGERS SYNDROME G Barnhill G., 2000, FOCUS AUTISM OTHER D, V15, P146, DOI [10.1177/108835760001500303, DOI 10.1177/108835760001500303] BETZ NE, 1987, J COUNS PSYCHOL, V34, P393, DOI 10.1037/0022-0167.34.4.393 BLAIR KA, 2003, 15 MENTAL MEASUREMEN FURLONG M, 1995, 12 MENTAL MEASUREMEN Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Gilliam J. E., 1995, GILLIAM AUTISM RATIN GILLIAM JE, 2001, GILLIAM ASPERGERS DI Gresham F. M., 1990, SOCIAL SKILLS RATING Howlin P., 2000, CHILD PSYCHOL PSYCHI, V5, P120, DOI DOI 10.1017/S1360641700002288 Klin A., 2000, ASPERGER SYNDROME, P309 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C., 1997, HDB AUTISM PERVASIVE, P460 Mayes SD, 2004, J DEV PHYS DISABIL, V16, P257, DOI 10.1023/B:JODD.0000032301.07550.0e Miller JN, 2000, J ABNORM PSYCHOL, V109, P227, DOI 10.1037/0021-843X.109.2.227 *MISS DEP ED, 2002, DEF EL CRIT DIS MYLES BS, 2001, ASPERGER SYNDROME DI Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 Ozonoff S, 2000, ASPERGER SYNDROME, P72 Prior M, 1998, J CHILD PSYCHOL PSYC, V39, P893, DOI 10.1111/1469-7610.00389 Schopler E., 1988, CHILDHOOD AUTISM RAT South M, 2002, J AUTISM DEV DISORD, V32, P593, DOI 10.1023/A:1021211232023 TANTAM D, 1988, J CHILD PSYCHOL PSYC, V29, P245, DOI 10.1111/j.1469-7610.1988.tb00713.x Volkmar FR, 2004, J CHILD PSYCHOL PSYC, V45, P135, DOI 10.1046/j.0021-9630.2003.00317.x Wing L, 1998, ASPERGER SYNDROME HI, P11 World Health Organization, 1993, ICD10 CLASS MENT BEH NR 30 TC 5 Z9 5 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1056-263X J9 J DEV PHYS DISABIL JI J. Dev. Phys. Disabil. PD JUN PY 2006 VL 18 IS 2 BP 163 EP 182 DI 10.1007/s10882-006-9008-6 PG 20 WC Rehabilitation SC Rehabilitation GA 102UW UT WOS:000241839800005 ER PT J AU Sumi, S Taniai, H Miyachi, T Tanemura, M AF Sumi, S Taniai, H Miyachi, T Tanemura, M TI Sibling risk of pervasive developmental disorder estimated by means of an epidemiologic survey in Nagoya, Japan SO JOURNAL OF HUMAN GENETICS LA English DT Article DE autism; pervasive developmental disorder; sibling; low birth-weight; multifactorial inheritance ID AUTISM; GENETICS; CHILDREN; TWIN AB Broad-spectrum autism, referred to as pervasive developmental disorder (PDD), may be associated with genetic factors. We examined 241 siblings in 269 Japanese families with affected children. The sibling incidence of PDD was 10.0% whereas the prevalence of PDD in the general population in the same geographic region was 2.1%. Both of these rates are higher than those reported previously, probably because of the expanded clinical criteria applied. The prevalence in males of the general population was 3.3% and that in females was 0.82%. The sibling incidences were 7.7 and 20.0% for families in which the probands were male and female, respectively. Because the reversed sex ratios correspond to the general rule for a multifactorial threshold model, we suggest that most PDD cases result from the cumulative effects of multiple factors (mostly genetic). The sibling incidences were 0 and 10.9% for families in which the proband had low and normal birth-weight, respectively, suggesting the risk is lower in families with low-birth-weight probands. C1 W Dist Care Ctr Disabled Children, Nakagawa Ku, Nagoya, Aichi 4540828, Japan. Nagoya City Univ, Grad Sch Med Sci, Dept Pediat Neonatol & Congenital Disorders, Nagoya, Aichi 467, Japan. Nagoya Child Welf Ctr, Dept Pediat, Nagoya, Aichi, Japan. Nagoya City Univ Hosp, Div Clin & Mol Genet, Nagoya, Aichi, Japan. RP Sumi, S (reprint author), W Dist Care Ctr Disabled Children, Nakagawa Ku, 20-48 Komoto, Nagoya, Aichi 4540828, Japan. EM satoshi-sumi@mbn.nifty.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 1980, DIAGN STAT MAN MENT AUGUST GJ, 1981, BRIT J PSYCHIAT, V138, P416, DOI 10.1192/bjp.138.5.416 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAIRD TD, 1985, J AUTISM DEV DISORD, V15, P315, DOI 10.1007/BF01531501 CARTER CO, 1969, BRIT MED BULL, V25, P52 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Cryan E, 1996, J AUTISM DEV DISORD, V26, P453, DOI 10.1007/BF02172829 Emery AEH, 1986, METHODOLOGY MED GENE Gillberg C., 2000, BIOL AUTISTIC SYNDRO Harper P. S., 2004, PRACTICAL GENETIC CO, P100 Honda H, 2005, J CHILD PSYCHOL PSYC, V46, P572, DOI 10.1111/j.1469-7610.2005.01425.x Icasiano F, 2004, J PAEDIATR CHILD H, V40, P696, DOI 10.1111/j.1440-1754.2004.00513.x Indredavik M. S., 2004, ARCH DIS CHILD-FETAL, V89, P445 Jamain S, 2003, NAT GENET, V34, P27, DOI 10.1038/ng1136 Jones MB, 2002, AM J MED GENET, V114, P558, DOI 10.1002/ajmg.10513 Penrose L. S., 1963, BIOL MENTAL DEFECT RITVO ER, 1985, AM J PSYCHIAT, V142, P74 RITVO ER, 1989, AM J PSYCHIAT, V146, P1032 Shastry BS, 2003, J HUM GENET, V48, P495, DOI 10.1007/s10038-003-0064-9 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x WING L, 1996, AUTISM SPECTRUM GUID NR 22 TC 30 Z9 32 PU SPRINGER TOKYO PI TOKYO PA 3-3-13, HONGO, BUNKYO-KU, TOKYO, 113-0033, JAPAN SN 1434-5161 J9 J HUM GENET JI J. Hum. Genet. PD JUN PY 2006 VL 51 IS 6 BP 518 EP 522 DI 10.1007/s10038-006-0392-7 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 056NX UT WOS:000238532300003 PM 16565880 ER PT J AU Ross, P Cuskelly, M AF Ross, Penelope Cuskelly, Monica TI Adjustment, sibling problems and coping strategies of brothers and sisters of children with autistic spectrum disorder SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article DE sibling; autism; autistic spectrum disorder; Asperger syndrome; coping; adjustment; relationship ID BEHAVIORAL-ADJUSTMENT; CHRONIC DISABILITIES; MENTAL-RETARDATION; ADOLESCENTS; CHECKLIST; IMPAIRMENT; COMPETENCE; AUSTRALIA; ILLNESS AB Background Siblings of children with autistic spectrum disorder (ASD) express more problem behaviours and experience more difficulties in their relationships than do children in families where all children are developing typically. We know little about what contributes to these difficulties. Method Mothers of a child with ASD completed the Child Behavior Checklist (Achenbach, 1991) with respect to a nondisabled sibling. Siblings responded to a questionnaire tapping their knowledge about their brother or sister's disorder. They reported on problems they had experienced with their brother or sister with ASD and on the coping strategies they had used in response to these events. Problems were classified into 1 of 5 problem types. Results Aggressive behaviour was the most commonly reported interaction problem and anger was the usual response. Siblings did not generally choose blaming (either self or other) as a coping strategy when facing difficulties with their brother or sister with ASD. Neither coping strategies nor knowledge of ASD were associated with adjustment. Forty percent of nondisabled siblings had scores on the Child Behavior Checklist that placed them in the borderline or clinical range. Conclusions The current study indicated that siblings of children with ASD are at increased risk of developing internalising behaviour problems. The contributing factors to this outcome are unknown at this point. It is important for research to focus on dynamic variables in the search for these contributors, as they are open to change. C1 Univ Queensland, Sch Educ, Brisbane, Qld 4072, Australia. RP Cuskelly, M (reprint author), Univ Queensland, Sch Educ, Brisbane, Qld 4072, Australia. EM m.cuskelly@uq.edu.au RI Cuskelly, Monica/A-6517-2011 OI Cuskelly, Monica/0000-0001-9986-9985 CR Achenbach TM, 1991, MANUAL CHILD BEHAV C American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAGENHOLM A, 1991, J MENT DEFIC RES, V35, P291 BOND L, 1994, AUST PSYCHOL, V29, P103, DOI 10.1080/00050069408257332 Cuskelly M., 1999, INT J ADV COUNS, V21, P111, DOI 10.1023/A:1005331700993 DONOVAN AM, 1988, AM J MENT RETARD, V92, P502 Edgar KA, 2003, J PEDIATR PSYCHOL, V28, P485, DOI 10.1093/jpepsy/jsg039 Fisman S, 1996, J AM ACAD CHILD PSY, V35, P1532, DOI 10.1097/00004583-199611000-00023 Fisman S, 2000, CAN J PSYCHIAT, V45, P369 Gamble W., 1989, J APPLIED DEV PSYCHO, V10, P353, DOI 10.1016/0193-3973(89)90035-X GAMBLE WC, 1993, EFFECTS OF MENTAL RETARDATION, DISABILITY AND ILLNESS ON SIBLING RELATIONSHIPS, P287 Garralda ME, 2004, J CHILD PSYCHOL PSYC, V45, P543 Gibbs B., 1993, FAMILIES DISABILITY, P343 Gilliam J. 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Intellect. Dev. Dis. PD JUN PY 2006 VL 31 IS 2 BP 77 EP 86 DI 10.1080/13668250600710864 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 072QO UT WOS:000239688300002 PM 16782592 ER PT J AU Kishida, Y Kemp, C AF Kishida, Yuriko Kemp, Coral TI A measure of engagement for children with intellectual disabilities in early childhood settings: A preliminary study SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article DE engagement; engagement measure; severe intellectual disability; children; childcare; inclusion ID CLASSROOM ACTIVITIES; EARLY INTERVENTION; AUTISM; PRESCHOOLERS; SUPPORT; TRIALS; CARE AB Background The purpose of this study was to develop a measure of engagement that could be used in practice with children with disabilities, including children with severe intellectual disabilities. Method The Individual Child Engagement Record (ICER) was designed to observe and record the engagement of individual children in order to identify optimal programs for them. Using the measure, 5 children with mild to severe disabilities were observed in an inclusive childcare setting across 4 types of ongoing activities: routine, one-to-one instruction, planned, and child-initiated. Results Generally, the children were better engaged in routine activities. The lowest level of engagement was found for planned activities. There were, however, differences across children with regard to the relative value of the different types of activities in promoting engagement. Conclusions The measure allowed for the identification of activities that would provide better learning opportunities for children with significant disabilities. C1 Macquarie Univ, Special Educ Ctr, N Ryde, NSW 2109, Australia. RP Kemp, C (reprint author), Macquarie Univ, Special Educ Ctr, N Ryde, NSW 2109, Australia. 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D., 1996, EARLY EDUC DEV, V7, P205, DOI 10.1027/s15566935eed0703_1 STRAIN PS, 1995, J EMOT BEHAV DISORD, V3, P108 VanDerHeyden AM, 2005, TOP EARLY CHILD SPEC, V25, P81, DOI 10.1177/02711214050250020501 Wolery M, 2002, TOP EARLY CHILD SPEC, V22, P131, DOI 10.1177/02711214020220030101 ZANOLLI K, 1995, BEHAV MODIF, V19, P339, DOI 10.1177/01454455950193005 NR 43 TC 11 Z9 11 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PD JUN PY 2006 VL 31 IS 2 BP 101 EP 114 DI 10.1080/13668250600710823 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 072QO UT WOS:000239688300005 PM 16782595 ER PT J AU Sahoo, T Peters, SU Madduri, NS Glaze, DG German, JR Bird, LM Barbieri-Welge, R Bichell, TJ Beaudet, AL Bacino, CA AF Sahoo, T Peters, SU Madduri, NS Glaze, DG German, JR Bird, LM Barbieri-Welge, R Bichell, TJ Beaudet, AL Bacino, CA TI Microarray based comparative genomic hybridization testing in deletion bearing patients with Angelman syndrome: genotype-phenotype correlations SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID HEREDITARY SPASTIC PARAPLEGIA; PRADER-WILLI-SYNDROME; CHROMOSOME 15Q11-Q13; AUTISTIC DISORDER; PARENTAL ORIGIN; GENE UBE3A; FRAGILE-X; MUTATIONS; 15Q; CHILDREN AB Background: Angelman syndrome (AS) is a neurodevelopmental disorder characterised by severe mental retardation, dysmorphic features, ataxia, seizures, and typical behavioural characteristics, including a happy sociable disposition. AS is caused by maternal deficiency of UBE3A (E6 associated protein ubiquitin protein ligase 3A gene), located in an imprinted region on chromosome 15q11-q13. Although there are four different molecular types of AS, deletions of the 15q11-q13 region account for approximately 70% of the AS patients. These deletions are usually detected by fluorescence in situ hybridisation studies. The deletions can also be subclassified based on their size into class I and class II, with the former being larger and encompassing the latter. Methods: We studied 22 patients with AS due to microdeletions using a microarray based comparative genomic hybridisation ( array CGH) assay to define the deletions and analysed their phenotypic severity, especially expression of the autism phenotype, in order to establish clinical correlations. Results: Overall, children with larger, class I deletions were significantly more likely to meet criteria for autism, had lower cognitive scores, and lower expressive language scores compared with children with smaller, class II deletions. Children with class I deletions also required more medications to control their seizures than did those in the class II group. Conclusions: There are four known genes (NIPA1, NIPA2, CYFIP1, & GCP5) that are affected by class I but not class II deletions, thus raising the possibility of a role for these genes in autism as well as the development of expressive language skills. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. San Diego Childrens Hosp, San Diego, CA USA. Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA. RP Bacino, CA (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. 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Med. Genet. PD JUN PY 2006 VL 43 IS 6 BP 512 EP 516 DI 10.1136/jmg.2005.036913 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 048UZ UT WOS:000237973300008 PM 16183798 ER PT J AU Jones, JD AF Jones, Jennifer D. TI Songs composed for use in music therapy: A survey of original songwriting practices of music therapists SO JOURNAL OF MUSIC THERAPY LA English DT Article; Proceedings Paper CT 11th World Congress of Music Therapy CY JUL 19-23, 2005 CL Brisbane, AUSTRALIA ID ADOLESCENTS; CHILDREN; PROGRAM; AUTISM; PEOPLE; LIVE AB While researchers have documented the efficacy of clinical songwriting in music therapy, limited research has been conducted on songs composed by music therapists that address clinical goals. The purpose of this research was to examine the original songwriting practices of music therapists. Professional music therapists (N = 1,364) received a 14-question survey via email asking each to identify client populations and clinical goals addressed by original songs, their length of time in clinical practice, and specifics about their acquisition of songwriting skills. The data collected from 302 completed surveys revealed that respondents who used original songs were most likely to work with children and adolescents in schools or the developmental disability field and wrote songs in order to individualize treatment. Music therapists working with persons over 65 years of age in long term care or assisted living programs were the least likely to use original songs in clinical practice, opting for interventions utilizing the client's familiar music. Most music therapists found songwriting generally easy, but only 37% indicated that they acquired this skill during their undergraduate degree. Additional research on the clinical efficacy of original songs and therapist's compositional processes is needed to identify best practices models for strategic songwriting. C1 Florida State Univ, Tallahassee, FL 32306 USA. RP Jones, JD (reprint author), Florida State Univ, Tallahassee, FL 32306 USA. CR *AMTA, 2004, AMTA MEMB SOURC Baker F, 2001, J MUSIC THER, V38, P170 Brownell MD, 2002, J MUSIC THER, V39, P117 BRUNK BK, 1990, SONGWRITING MUSIC TH Cordobes TK, 1997, J MUSIC THER, V34, P46 EDGERTON CD, 1990, MUSIC THERAPY PERSPE, V8, P15 EDWARDS J, 1998, MUSIC THERAPY PERSPE, V16, P21 FARNAN LA, 1987, MUSIC THERAPY PERSPE, V4, P8 FICKEN T, 1976, J MUSIC THER, V13, P163 FREED BS, 1987, MUSIC THERAPY PERSPE, V4, P13 Fulford M., 2002, MUSIC THERAPY PERSPE, V20, P112 GALIZIO M, 1972, J APPL SOC PSYCHOL, V2, P350, DOI 10.1111/j.1559-1816.1972.tb01286.x Gallagher L. 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M., 2000, EFFECTIVENESS MUSIC, P1 Walworth DD, 2003, J MUSIC THER, V40, P2 Whipple J, 2004, J MUSIC THER, V41, P90 NR 32 TC 2 Z9 2 PU NATL ASSOC MUSIC THERAPY INC PI SILVER SPRING PA 8455 COLESVILLE RD, STE 1000, SILVER SPRING, MD 20910 USA SN 0022-2917 J9 J MUSIC THER JI J. Music Ther. PD SUM PY 2006 VL 43 IS 2 BP 94 EP 110 PG 17 WC Music; Rehabilitation SC Music; Rehabilitation GA 065JP UT WOS:000239156400001 PM 16854214 ER PT J AU Simonneau, MJ Maussion, G Bestel, AM Moalic, JM Gorwood, P Ramoz, N AF Simonneau, MJ Maussion, G Bestel, AM Moalic, JM Gorwood, P Ramoz, N TI Dysregulation of genes encoding synaptic proteins in autism: analysis of identified subgroups of neurons from human brain using Q-PCR SO JOURNAL OF NEURAL TRANSMISSION LA English DT Meeting Abstract C1 Univ Paris 07, Unite INSERM 675, IFR2, Paris, France. NR 0 TC 0 Z9 0 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PD JUN PY 2006 VL 113 IS 6 BP XV EP XV PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 050PM UT WOS:000238100400066 ER PT J AU Brown, KE Mirenda, P AF Brown, Kenneth E. Mirenda, Pat TI Contingency mapping: Use of a novel visual support strategy as an adjunct to functional equivalence training SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID POSITIVE BEHAVIOR SUPPORT; PHOTOGRAPHIC ACTIVITY SCHEDULES; DESTRUCTIVE BEHAVIOR; ALTERNATIVE BEHAVIOR; COMPONENT ANALYSIS; REINFORCEMENT; AUTISM; EXTINCTION; INTERVENTION; MAINTENANCE AB This study evaluated the effectiveness of contingency mapping, a new visual support strategy designed to enhance clients' understanding of the contingencies associated with functional equivalence training (FET). The study was conducted in a general education classroom with an adolescent boy with autism who engaged in prompt dependent behavior. A multiple baseline ABCD design across three activities was used to evaluate intervention effectiveness and to compare a verbal contingency intervention with contingency mapping. Results indicated that the verbal contingency had no effect, whereas contingency mapping was related to immediate, dramatic, and sustained reductions in problem behavior and increases in alternative behavior. Social validation and follow-up data are also included. The potential of contingency mapping as an adjunct to FET is discussed. C1 Univ British Columbia, Vancouver, BC V5Z 1M9, Canada. RP Brown, KE (reprint author), 939 Ridgeway Ave, Vancouver, BC V7L 3R3, Canada. EM kennethbrown@telus.net CR Baker M. 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PD SUM PY 2006 VL 8 IS 3 BP 155 EP 164 DI 10.1177/10983007060080030401 PG 10 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 063VF UT WOS:000239047300004 ER PT J AU Mechling, LC AF Mechling, Linda C. TI Comparison of the effects of three approaches on the frequency of stimulus activations, via a single switch, by students with profound intellectual disabilities SO JOURNAL OF SPECIAL EDUCATION LA English DT Article ID MULTIPLE DISABILITIES; MODERATE DISABILITIES; PREFERENCES; MICROSWITCHES; CHILDREN; AUTISM; INSTRUCTION; HANDICAPS; SKILLS AB The effects of three classes of reinforcing stimuli were compared across three students with profound intellectual disabilities. A multielement design with no baseline and final "best treatments" phase was used to measure the frequency of single-switch activations by each student across treatments. The three interventions were Treatment A, adapted toys and devices; Treatment B, cause-and-effect commercial software; and Treatment C, instructor-created video programs. Stimulus activations using a single switch were consistently greater when using individualized computer-based video programs. Implications for identifying stimuli for students who may not respond to traditional methods for teaching means-end contingencies (cause and effect) are discussed. C1 Univ N Carolina, Dept Curricular Studies, Wilmington, NC 28403 USA. RP Mechling, LC (reprint author), Univ N Carolina, Dept Curricular Studies, 601 S Coll Rd, Wilmington, NC 28403 USA. CR Alberto P. 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W., 1993, INFANTS YOUNG CHILDR, V5, P58 Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 *VORT CORP, 1997, HAW EARL LEARN PROF WACKER DP, 1988, J APPL BEHAV ANAL, V21, P331, DOI 10.1901/jaba.1988.21-331 WACKER DP, 1985, J APPL BEHAV ANAL, V18, P173, DOI 10.1901/jaba.1985.18-173 YORK J, 1985, J ASSOC PERS SEVERE, V10, P214 NR 46 TC 36 Z9 36 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0022-4669 J9 J SPEC EDUC JI J. Spec. Educ. PD SUM PY 2006 VL 40 IS 2 BP 94 EP 102 DI 10.1177/00224669060400020501 PG 9 WC Education, Special SC Education & Educational Research GA 066YN UT WOS:000239266800003 ER PT J AU Kashinath, S Woods, J Goldstein, H AF Kashinath, S Woods, J Goldstein, H TI Enhancing generalized teaching strategy use in daily routines by parents of children with autism SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE language treatment; autism; preschool children ID YOUNG-CHILDREN; DEVELOPMENTAL DELAYS; MATERNAL LANGUAGE; SKILLS; INTERVENTION; ACQUISITION; MOTHERS; STYLE; COMMUNICATION; DISABILITIES AB Purpose: The purpose of this study was to examine the effects of facilitating generalized use of teaching strategies by parents of children with autism within daily routines. Method: Five preschool children with autism participated in intervention with a parent within daily routines in the family's home. Parents learned to include 2 teaching strategies in target routines to address their child's communication objectives. Parent-child interactions in routines were videotaped for data coding and analysis. Proactive programming of generalization occurred by systematic selection of intervention routines and by embedding intervention in multiple routines. Generalization data were collected by measuring strategy use in untrained routines. A multiple baseline design across teaching strategies was used to assess experimental effects. Results: All parents demonstrated proficient use of teaching strategies and generalized their use across routines. The intervention had positive effects on child communication outcomes. All parents perceived the intervention to be beneficial. Conclusion: Results from this study add to the limited body of evidence supporting parent-implemented interventions in natural environments with young children with autism spectrum disorder. 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Speech Lang. Hear. Res. PD JUN PY 2006 VL 49 IS 3 BP 466 EP 485 DI 10.1044/1092-4388(2006/036) PG 20 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 056IG UT WOS:000238515100001 PM 16787891 ER PT J AU Arent, SM Schmitz, S AF Arent, SM Schmitz, S TI Exercise as a means to reduce stereotypic behaviors among children and adolescents with autism SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract C1 Rutgers State Univ, Piscataway, NJ 08855 USA. NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2006 VL 28 SU S BP S27 EP S27 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 050ZV UT WOS:000238130900050 ER PT J AU Ronald, A Happe, F Bolton, P Butcher, LM Price, TS Wheelwright, S Baron-Cohen, S Plomin, R AF Ronald, Angelica Happe, Francesca Bolton, Patrick Butcher, Lee M. Price, Thomas S. Wheelwright, Sally Baron-Cohen, Simon Plomin, Robert TI Genetic heterogeneity between the three components of the autism spectrum: A twin study SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE twins; genetics; autism spectrum disorders ID RECIPROCAL SOCIAL-BEHAVIOR; CAST CHILDHOOD ASPERGER; INDIVIDUAL-DIFFERENCES; CHILDREN; TRAITS; MULTIVARIATE; LANGUAGE AB Objective: This study investigated the etiology of autistic-like traits in the general population and the etiological overlap between the three aspects of the triad of impairments (social impairments, communication impairments, restricted repetitive behaviors and interests) that together define autism spectrum disorders. Method: Parents of 3,400 8-year-old twin pairs from the Twins Early Development Study completed the Childhood Asperger Syndrome Test, a screening instrument for autism spectrum symptoms in mainstream samples. Genetic model-fitting of categorical and continuous data is reported. Results: High heritability was found for extreme autistic-like traits (0.64-0.92 for various cutoffs) and autistic-like traits as measured on a continuum (0.78-0.81), with no significant shared environmental influences. All three subscales were highly heritable but showed low covariation. In the genetic modeling, distinct genetic influences were identified for the three components. Conclusions: These results suggest the triad of impairments that define autism spectrum disorders is heterogeneous genetically. Molecular genetic research examining the three components separately may identify different causal pathways for the three components. The analyses give no indication that different genetic processes affect extreme autistic impairments and autistic impairments as measured on a continuum, but this can only be directly tested once genes are identified. C1 Kings Coll London, Social Genet & Dev Psychiat Ctr, Inst Psychiat, London SE5 8AF, England. Univ Penn, Sch Med, Inst Translat Med & Therapeut, Philadelphia, PA 19104 USA. Univ Cambridge, Autism Res Ctr, Cambridge, England. RP Ronald, A (reprint author), Kings Coll London, Social Genet & Dev Psychiat Ctr, Inst Psychiat, De Crespigny Pk, London SE5 8AF, England. EM a.ronald@iop.kcl.ac.uk RI Butcher, Lee/C-1540-2008; Happe, Francesca/D-5544-2012; Ronald, Angelica/C-7812-2009; Plomin, Robert/B-8911-2008; Price, Thomas/B-7372-2008; Bolton, Patrick/E-8501-2010 OI Ronald, Angelica/0000-0002-9576-2176; Price, Thomas/0000-0001-7356-2109; Bolton, Patrick/0000-0002-5270-6262 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAILEY A, 1995, PSYCHOL MED, V25, P695 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Cohen J., 1988, STAT POWER ANAL BEHA, V2nd Constantino JN, 2003, J AUTISM DEV DISORD, V33, P427, DOI 10.1023/A:1025014929212 Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Constantino JN, 2000, J DEV BEHAV PEDIATR, V21, P2 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 DEFRIES JC, 1988, ACTA GENET MED GEMEL, V37, P205 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Loat CS, 2004, TWIN RES, V7, P54, DOI 10.1375/13690520460741444 Loehlin JC, 1996, BEHAV GENET, V26, P65, DOI 10.1007/BF02361160 NEALE MC, 2003, MX STAT MODELING PLOMIN R, 1994, SCIENCE, V264, P1733, DOI 10.1126/science.8209254 Plomin R, 2001, BEHAV GENETICS Price T S, 2000, Twin Res, V3, P129, DOI 10.1375/136905200320565391 Purcell S, 2003, BEHAV GENET, V33, P271, DOI 10.1023/A:1023494408079 Ronald A, 2005, DEVELOPMENTAL SCI, V8, P444, DOI 10.1111/j.1467-7687.2005.00433.x Rutter M., 2003, SOCIAL COMMUNICATION Saudino K J, 2000, Twin Res, V3, P224 Scott FJ, 2002, AUTISM, V6, P9, DOI 10.1177/1362361302006001003 Scourfield J, 1999, BRIT J PSYCHIAT, V175, P559, DOI 10.1192/bjp.175.6.559 SHROUT PE, 1979, PSYCHOL BULL, V86, P420, DOI 10.1037//0033-2909.86.2.420 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Sung YJ, 2005, AM J HUM GENET, V76, P68, DOI 10.1086/426951 Trouton A, 2002, TWIN RES, V5, P444, DOI 10.1375/136905202320906255 Williams J, 2005, AUTISM, V9, P45, DOI 10.1177/136261305049029 WING L, 1981, J AUTISM DEV DISORD, V11, P31, DOI 10.1007/BF01531339 NR 30 TC 205 Z9 209 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JUN PY 2006 VL 45 IS 6 BP 691 EP 699 DI 10.1097/01.chi.0000215325.13058.9d PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 046CE UT WOS:000237788200010 PM 16721319 ER PT J AU Dell, ML AF Dell, ML TI Handbook of autism and pervasive developmental disorders: Diagnosis, development, neurobiology, and behavior, 3rd edition, vol 1-2. SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Book Review C1 Emory Univ, Sch Med, Atlanta, GA 30322 USA. RP Dell, ML (reprint author), Emory Univ, Sch Med, Atlanta, GA 30322 USA. CR VOLKMAR FR, 2005, HANDBOOK AUTISM PERV, V2 VOLKMAR FR, 2005, HANDBOOK AUTISM PERV, V1 NR 2 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JUN PY 2006 VL 45 IS 6 BP 759 EP 761 DI 10.1097/01.chi.0000228313.45159.0a PG 3 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 046CE UT WOS:000237788200020 ER PT J AU Seckington, C AF Seckington, C TI Autism spectrum disorders and visual impairment. Meeting students learning needs. SO JOURNAL OF VISUAL IMPAIRMENT & BLINDNESS LA English DT Book Review C1 Maryland Sch Blind, Expanded Acad Program, Baltimore, MD 21236 USA. RP Seckington, C (reprint author), Maryland Sch Blind, Expanded Acad Program, 3501 Taylor Ave, Baltimore, MD 21236 USA. EM csecki@pco.edu CR Gense M. H., 2005, AUTISM SPECTRUM DISO NR 1 TC 0 Z9 0 PU AMER FOUNDATION BLIND PI NEW YORK PA J VISUAL IMPAIRMENT BLINDNESS 11 PENN PLAZA SUITE 300, NEW YORK, NY 10001 USA SN 0145-482X J9 J VISUAL IMPAIR BLIN JI J. Vis. Impair. Blind. PD JUN PY 2006 VL 100 IS 6 BP 377 EP 378 PG 2 WC Rehabilitation SC Rehabilitation GA 056HW UT WOS:000238514000008 ER PT J AU Geier, DA Geier, MR AF Geier, DA Geier, MR TI An assessment of downward trends in neurodevelopmental disorders in the United States following removal of thimerosal from childhood vaccines SO MEDICAL SCIENCE MONITOR LA English DT Article DE autism spectrum disorder; merthiolate; Thimerasol; Thiomersal ID EVENT REPORTING SYSTEM; DEVELOPMENTAL DISORDERS; CAUSAL ASSOCIATION; ADVERSE EVENTS; UP ANALYSIS; CELL-DEATH; AUTISM; PREVALENCE; MERCURY; POPULATION AB Background: The US is in the midst of an epidemic of neurodevelopmental disorders (NDs). Thimerosal is an ethylmercury-containing compound added to some childhood vaccines. Several previous epidemiological studies conducted in the US have associated Thimerosal-containing vaccine (TCV) administration with NDs. Material/Methods: An ecological study was undertaken to evaluate NDs reported to the Vaccine Adverse Event Reporting System (VAERS) from 1991 through 2004 by date of receipt and by date of vaccine administration. The NDs examined included autism, mental retardation, and speech disorders. Statistical trend analysis was employed to evaluate the effects of removal of Thimerosal on the proportion of NDs reported to VAERS. Results: There was a peak in the proportion of ND reports received by VAERS in 2001-2002 and in the proportion of ND reports by date of vaccine administration in 1998. There were significant reductions in the proportion of NDs reported to VAERS as Thimerosal was begun to be removed from childhood vaccines in the US from mid-1999 onwards. Conclusions: The present study provides the first epidemiological evidence showing that as Thimerosal was removed from childhood vaccines, the number of NDs has decreased in the US. The analysis techniques utilized attempted to minimize chance or bias/confounding. Additional research should be conducted to further evaluate the relationship between TCVs and NDs. This is especially true because the handling of vaccine safety data from the National Immunization Program of the CDC has been called into question by the Institute of Medicine of the National Academy of Sciences in 2005. C1 Genet Ctr Amer, Silver Spring, MD 20905 USA. George Washington Univ, Dept Biochem, Washington, DC USA. RP Geier, MR (reprint author), Genet Ctr Amer, 14 Redgate Ct, Silver Spring, MD 20905 USA. 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Sci. Monitor PD JUN PY 2006 VL 12 IS 6 BP CR231 EP CR239 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 056RE UT WOS:000238542000005 PM 16733480 ER PT J AU Sugden, C AF Sugden, C. TI One-carbon metabolism in psychiatric illness SO NUTRITION RESEARCH REVIEWS LA English DT Review DE methylation; epigenetics; psychiatric illness; autism; one-carbon metabolism; S-adenosylmethionine ID CATECHOL-O-METHYLTRANSFERASE; SERUM CREATINE-PHOSPHOKINASE; PHOSPHATIDYLETHANOLAMINE N-METHYLTRANSFERASE; ELEVATED HOMOCYSTEINE LEVELS; ADENOSYL-L-METHIONINE; METHYLENETETRAHYDROFOLATE REDUCTASE; FOLIC-ACID; PLASMA HOMOCYSTEINE; PHOSPHOLIPID METHYLATION; SCHIZOPHRENIC-PATIENTS AB The cost of psychiatric illness to the UK economy was recently estimated at 77 pound billion annually. Despite years of research no firm aetiological explanation exists, and with no physiological or biochemical markers diagnosis is made entirely on a behavioural basis. All current pharmacological therapies are associated with serious long-term side effects. Substantial evidence supports the involvement of one-carbon cycle dysregulation in psychiatric illness, but this is not currently used as a basis for diagnosis or treatment. The present paper reviews the evidence for one-carbon cycle dysregulation in schizophrenic, bipolar, depressed and autistic patients. Also presented are novel findings from the field of epigenetics, which demonstrate how the one-carbon cycle-derived methyl donor S-adenosylmethionine influences the expression of key genes in the brain affecting memory, learning, cognition and behaviour, genes whose expression is reduced to varying degrees in these patient groups. Clinical evidence that nutritional supplements can rectify one-carbon cycle activity, and restore normal gene expression, suggests a novel approach to the development of biochemical tests and simple, non-harmful treatments for some psychiatric patients. Conversely, evidence from animal studies highlights the dangers of exposing the unborn fetus to very high dietary levels of folic acid, a one-carbon cycle cofactor. Fetal adaptations to a high-folate environment may interfere with folate metabolism postnatally, with serious consequences for the epigenetic regulation of gene expression. The public health implications of these diverse scenarios indicate an urgent need for further research in this field. C1 Univ Surrey, Ctr Nutr & Food Safety, Sch Biomed & Mol Sci, Guildford GU2 7XH, Surrey, England. RP Sugden, C (reprint author), Univ Surrey, Ctr Nutr & Food Safety, Sch Biomed & Mol Sci, Guildford GU2 7XH, Surrey, England. 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Res. Rev. PD JUN PY 2006 VL 19 IS 1 BP 117 EP 136 DI 10.1079/NRR2006119 PG 20 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 067EE UT WOS:000239283700010 PM 19079880 ER PT J AU Singh, VK Hanson, J AF Singh, VK Hanson, J TI Assessment of metallothionein and antibodies to metallothionein in normal and autistic children having exposure to vaccine-derived thimerosal SO PEDIATRIC ALLERGY AND IMMUNOLOGY LA English DT Article DE autism; metallothionein; autoimmunity; mercury; thimerosal; immunotoxicity ID MERCURY; AUTOIMMUNITY; INDUCTION; CADMIUM; CHLORIDE; PROTEIN; RATS; MICE AB Allergic autoimmune reaction after exposure to heavy metals such as mercury may play a causal role in autism, a developmental disorder of the central nervous system. As metallothionein (MT) is the primary metal-detoxifying protein in the body, we conducted a study of the MT protein and antibodies to metallothionein (anti-MT) in normal and autistic children whose exposure to mercury was only from thimerosal-containing vaccines. Laboratory analysis by immunoassays revealed that the serum level of MT did not significantly differ between normal and autistic children. Furthermore, autistic children harboured normal levels of anti-MT, including antibodies to isoform MT-I (anti-MT-I) and MT-II (anti-MT-II), without any significant difference between normal and autistic children. Our findings indicate that because autistic children have a normal profile of MT and anti-MT, the mercury-induced autoimmunity to MT may not be implicated in the pathogenesis of autism. C1 Utah State Univ, Dept Biol, Logan, UT 84322 USA. RP Singh, VK (reprint author), Utah State Univ, Dept Biol, 5305 Old Main Hill, Logan, UT 84322 USA. 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Allergy Immunol. PD JUN PY 2006 VL 17 IS 4 BP 291 EP 296 DI 10.1111/j.1399-3038.2005.00348.x PG 6 WC Allergy; Immunology; Pediatrics SC Allergy; Immunology; Pediatrics GA 050CG UT WOS:000238064500008 PM 16771783 ER PT J AU Blanchard, LT Gurka, MJ Blackman, JA AF Blanchard, LT Gurka, MJ Blackman, JA TI Emotional, developmental, and behavioral health of American children and their families: A report from the 2003 National Survey of Children's Health SO PEDIATRICS LA English DT Article DE development; behavior; emotional status; Survey of Children's Health ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; EATING-DISORDERS; PARENTS CONCERNS; SUBSTANCE-ABUSE; CARE NEEDS; PREVALENCE; AUTISM; DISABILITIES; ADOLESCENTS; POPULATION AB BACKGROUND. Recent children's health surveys have documented a high prevalence of emotional, developmental, and behavioral problems among children. Data from the 2003 National Survey of Children's Health provide new insights into these problems and their association with family function and community participation. These issues have become a current focus of the World Health Organization. METHODS. Answers to questions of interest from the 2003 National Survey of Children's Health were reported using estimates and SEs of rates. Statistical comparisons of rates with chi(2) tests at the 0.05 level were made when relevant. RESULTS. The most commonly diagnosed problems among children 6 - 17 years of age were learning disabilities (11.5%), attention-deficit/hyperactivity disorder (8.8%), and behavioral problems (6.3%); among preschoolers, speech problems (5.8%) and developmental delay (3.2%) were most common. One in 200 children was diagnosed with autism. In contrast, rates of parental concerns about emotional, developmental, or behavioral problems were much higher; for example, 41% of parents had concerns about learning difficulties and 36% about depression or anxiety. Children with developmental problems had lower self-esteem, more depression and anxiety, more problems with learning, missed more school, and were less involved in sports and other community activities. Their families experienced more difficulty in the areas of childcare, employment, parent-child relationships, and caregiver burden. CONCLUSIONS. The most recent National Survey of Children's Health mirrored results of previous surveys regarding rates of diagnosed emotional, developmental, and behavioral problems, including an escalating diagnosis of autism among children. Reported rates of parental concerns about these problems were much higher, suggesting possible underdiagnosis of children's problems. Children with chronic problems had diminished family functioning, more school absences, and less participation in community activities compared with other children. Their parents experienced more difficulty with childcare, employment, and parenting skills. A change in treatment emphasis is needed, away from an exclusive focus on a child's developmental and behavioral problems to one that addresses the impacts of these problems on the family and community participation. A new approach to the way these issues are addressed and managed has the potential to enhance the quality of life for a child, as well as the parents, and to produce more meaningful and tangible solutions to these complex and increasingly evident problems. C1 Univ Virginia, Dept Pediat, Charlottesville, VA USA. Univ Virginia, Dept Publ Hlth Sci, Charlottesville, VA USA. RP Blackman, JA (reprint author), Univ Virginia, Childrens Hosp, Kluge Childrens Rehabil Ctr, 2270 Ivy Rd, Charlottesville, VA 22903 USA. 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The purpose of this work was to develop a consensus statement on the current status and future role for pharmacologic management of insomnia in children and adolescents. METHOD. The National Sleep Foundation, in collaboration with Best Practice Project Management, Inc, convened expert representatives involved in the study and treatment of pediatric insomnia and conducted a 2-day conference to examine the role of pharmacologic management of pediatric insomnia and to make recommendations regarding the development of clinical trials in this area. After a series of presentations providing background on the current knowledge of pediatric insomnia and its treatment alternatives, workgroups provided recommendations for the evaluation of pharmacologic treatment of insomnia in specific populations of children and adolescents and developed guidelines for the core methodologic issues relevant to the design of clinical trials. The group developed consensus recommendations for clinical trials in this area encompassing: (1) high-priority patient populations for research, (2) inclusion/exclusion criteria, (3) outcome measures, (4) ethical considerations unique to clinical trials involving children and adolescents, and (5) priorities for future research that will enhance the understanding of pediatric insomnia. RESULTS. Conference participants unanimously agreed that there is a need for pharmacologic management of pediatric insomnia. Furthermore, the widespread use of "hypnotic" and psychotropic medications for children in the absence of safety and efficacy data indicates a knowledge gap about the best pharmacologic practices for management of pediatric insomnia. Attendees reached consensus on methodologic issues in the study of pharmacologic treatment of pediatric insomnia including agreeing on a definition of pediatric insomnia as "repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite age-appropriate time and opportunity for sleep and results in daytime functional impairment for the child and/or family." It was agreed that priority should be given to insomnia studies in children with attention-deficit/hyperactivity disorder and those with pervasive developmental disorders/autism spectrum disorder. There was also agreement on the need for pharmacokinetic and pharmacodynamic studies to determine appropriate dose levels and to evaluate safety with a wide range of doses. CONCLUSIONS. The treatment of pediatric insomnia is an unmet medical need. Before appropriate pharmacologic management guidelines can be developed, rigorous, large-scale clinical trials of pediatric insomnia treatment are vitally needed to provide information to the clinician on the safety and efficacy of prescription and over-the-counter agents for the management of pediatric insomnia. C1 St Josephs Univ, Dept Psychol, Philadelphia, PA 19131 USA. Childrens Hosp Philadelphia, Sleep Ctr, Philadelphia, PA USA. Univ Texas, SW Med Ctr, Dept Psychiat, Dallas, TX USA. Case Western Reserve Univ, Sch Med, Dept Pediat, Cleveland, OH 44106 USA. Yale Univ, Sch Med, Dept Pediat, Child Hlth Res Ctr, New Haven, CT USA. Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. Loyola Univ, Med Ctr, Dept Psychiat, Chicago, IL USA. Loyola Univ, Med Ctr, Dept Neurosci, Chicago, IL USA. Oregon Hlth & Sci Univ, Dept Psychiat, Portland, OR USA. Oregon Hlth & Sci Univ, Dept Pediat, Portland, OR USA. Med Consultant, Evanston, IL USA. Henry Ford Hosp, Sleep Disorders & Res Ctr, Detroit, MI USA. RP Mindell, JA (reprint author), St Josephs Univ, Dept Psychol, Philadelphia, PA 19131 USA. 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Measurement of urinary creatinine is commonly used to correct for total urine concentration. Various quantitative measures of compounds suspected to be either pathological to, or indicative of, possible therapeutic interventions for Pervasive Developmental Disorders (PDD) have relied extensively on spot creatinine as a ratio quantity, although this important metabolite has not been exclusively studied within this population. Levels of urinary creatinine in spot urine samples were analyzed for a group of children diagnosed with PDD (n = 24; median age, 75 months; range, 39-137 months) and a control group (n = 50; median age, 109 months; range, 59-140 months). Diagnosis of PDD was confirmed using the Autism Diagnostic Interview-Revised. Samples were collected and analyzed blind for creatinine content using an improved Jaffe's reaction method. Controlling for sample pH and body mass index, a significant decrease in urinary creatinine concentration was found in the PDD group compared to controls using a Mann-Whitney two-tailed ranks test (P = 0.001). Further studies of protein catabolism and renal function in autism are required to ascertain the relevance of decreased spot urinary creatinine excretion identified in this preliminary study. Issues regarding the use of single urine creatinine measurements and associated confounding variables are discussed in light of the findings, together with recommendations to use other internal or external standards for the quantification of urinary compounds in PDD research. C1 Univ Sunderland, Sch Hlth Nat & Social Sci, Autism Res Unit, Sunderland SR1 3SD, Durham, England. RP Whiteley, P (reprint author), Univ Sunderland, Sch Hlth Nat & Social Sci, Autism Res Unit, Sunderland SR1 3SD, Durham, England. 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Welsh, Marilyn TI Theory of mind and executive function: Working-memory capacity and inhibitory control as predictors of false-belief task performance SO PERCEPTUAL AND MOTOR SKILLS LA English DT Article ID INDIVIDUAL-DIFFERENCES; FUNCTION DEFICITS; CHILDRENS THEORY; YOUNG-CHILDREN; AUTISM; PERSPECTIVE; COMPLEXITY; DECEPTION; RESOURCES; CHILDHOOD AB This study of the relationship between theory of mind and executive function examined whether on the false-belief task age differences between 3 and 5 years of age are related to development of working-memory capacity and inhibitory processes. 72 children completed tasks measuring false belief, working memory, and inhibition. Significant age effects were observed for false-belief and working-memory performance, as well as for the false-alarm and perseveration measures of inhibition. A simultaneous multiple linear regression specified the contribution of age, inhibition, and working memory to the prediction of false-belief performance. 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Skills PD JUN PY 2006 VL 102 IS 3 BP 819 EP 835 DI 10.2466/PMS.102.3.819-835 PG 17 WC Psychology, Experimental SC Psychology GA 071BZ UT WOS:000239573700021 PM 16916162 ER PT J AU Nakahachi, T Iwase, M Takahashi, H Honaga, E Sekiyama, R Ukai, S Ishii, R Ishigami, W Kajimoto, O Yamashita, K Hashimoto, R Tanii, H Shimizu, A Takeda, M AF Nakahachi, T Iwase, M Takahashi, H Honaga, E Sekiyama, R Ukai, S Ishii, R Ishigami, W Kajimoto, O Yamashita, K Hashimoto, R Tanii, H Shimizu, A Takeda, M TI Discrepancy of performance among working memory-related tasks in autism spectrum disorders was caused by task characteristics, apart from working memory, which could interfere with task execution SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE autism spectrum disorders; digit span; digit symbol; vagueness; working memory ID HIGH-FUNCTIONING AUTISM; CARD SORTING TEST; IMPAIRED MEMORY; YOUNG-CHILDREN; SCHIZOPHRENIA; DYSFUNCTION; ATTENTION; SYMPTOMS; VALIDITY; BEHAVIOR AB Working memory performance has been inconsistently reported in autism spectrum disorders (ASD). Several studies in ASD have found normal performance in digit span and poor performance in digit symbol task although these are closely related with working memory. It is assumed that poor performance in digit symbol could be explained by confirmatory behavior, which is induced due to the vague memory representation of number-symbol association. Therefore it was hypothesized that the performance of working memory task, in which vagueness did not cause confirmatory behavior, would be normal in ASD. For this purpose, the Advanced Trail Making Test (ATMT) was used. The performance of digit span, digit symbol and ATMT was compared between ASD and normal control. The digit span, digit symbol and ATMT was given to 16 ASD subjects and 28 IQ-, age- and sex-matched control subjects. The scores of these tasks were compared. A significantly lower score for ASD was found only in digit symbol compared with control subjects. There were no significant difference in digit span and working memory estimated by ATMT. Discrepancy of scores among working memory-related tasks was demonstrated in ASD. Poor digit symbol performance, normal digit span and normal working memory in ATMT implied that ASD subjects would be intact in working memory itself, and that superficial working memory dysfunction might be observed due to confirmatory behavior in digit symbol. Therefore, to evaluate working memory in ASD, tasks that could stimulate psychopathology specific to ASD should be avoided. C1 Osaka Univ, Grad Sch Med, Dept Clin Neurosci, Suita, Osaka 5650871, Japan. Osaka Second Police Hosp, Osaka, Japan. Osakafu Eiseikai Clin, Osaka, Japan. Osaka Univ Foreign Studies, Osaka, Japan. Yamamoto Clin, Yonago, Tottori, Japan. Mie Univ, Dept Psychiat, Tsu, Mie, Japan. Natl Inst Neurosci, Tokyo, Japan. RP Nakahachi, T (reprint author), Osaka Univ, Grad Sch Med, Dept Clin Neurosci, D3 2-2 Yamadaoka, Suita, Osaka 5650871, Japan. 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Neurosci. PD JUN PY 2006 VL 60 IS 3 BP 312 EP 318 DI 10.1111/j.1440-1819.2006.01507.x PG 7 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 042GB UT WOS:000237514800008 PM 16732747 ER PT J AU Kurita, H Koyama, T AF Kurita, H Koyama, T TI Autism-Spectrum Quotient Japanese version measures mental health problems other than autistic traits SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE Autism Spectrum Quotient Japanese version (AQ-J); GHQ-12; mental health; pervasive developmental disorders (PDD); questionnaire ID QUESTIONNAIRE; POPULATION; DISORDERS; VALIDITY; AQ AB The purpose of the present paper was to examine the extent to which the Autism Spectrum Quotient Japanese version (AQ-J) measures mental health problems other than autistic traits, with the 12-item General Health Questionnaire Japanese version (GHQ-12) as a criterion. A questionnaire involving AQ-J and GHQ-12 was sent to 2000 adults aged 20-39 randomly selected from the general population, and intact data were obtained from 215 (mean age, 30.4 years; 86 male). The AQ-J score was significantly associated with the GHQ-12 score (r = 0.518) and was significantly higher in 111 scoring >= 4 on the GHQ-12 (mean = 24.8 +/- 6.5) than in 104 scoring < 4 (mean = 19.4 +/- 5.5). At a cut-off 22, the AQ-J had modest sensitivity (0.64) and specificity (0.66) for predicting mental health problems. The 21-item mental health AQ-J (AQJ-21MH; range, 0-21; cut-off, 9; sensitivity, 0.69; specificity, 0.76), items of which had a significant odds ratio (OR) for GHQ-12 >= 4, and the AQ-J-4MH (range, 0-4; cut-off, 2; sensitivity, 0.68; specificity, 0.74) consisting of four items with a significant OR adjusted for collinearity selected from the 21 items by multiple logistic regression, were more efficient than the AQ-J. Because the AQ-J and its short forms measure mental health problems other than autistic traits, it is important to consider such problems in interpreting AQ-J scores to identify persons who may need professional help when screening normally intelligent adolescents and adults with pervasive developmental disorders. C1 Zenkoku Ryoiku Sodan Ctr, Shinjuku Ku, Tokyo 1620051, Japan. Univ Tokyo, Grad Sch Med, Dept Mental Hlth, Tokyo, Japan. RP Kurita, H (reprint author), Zenkoku Ryoiku Sodan Ctr, Shinjuku Ku, 2-2-8 Nishiwaseda, Tokyo 1620051, Japan. EM hkurita@mvf.biglobe.ne.jp CR Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Doi Y, 2003, PSYCHIAT CLIN NEUROS, V57, P379, DOI 10.1046/j.1440-1819.2003.01135.x Fukunishi I, 1990, SHINRI RINSHO, V3, P228 Goldberg DP, 1997, PSYCHOL MED, V27, P191, DOI 10.1017/S0033291796004242 IWATA N, 1988, ENV SCI HOKKAIDO U, V11, P1 KAGEYAMA T, 2001, JPN J MENT HLTH, V16, P69 Kurita H, 2005, PSYCHIAT CLIN NEUROS, V59, P490, DOI 10.1111/j.1440-1819.2005.01403.x Kurita H, 2003, JPN J CLIN PSYCHIAT, V32, P1235 Kurumatani T, 2004, SOC PSYCH PSYCH EPID, V39, P402, DOI 10.1007/s00127-004-0758-0 Nakagawa Y, 1985, MANUAL JAPANESE VERS NIIRO M, 2001, SEISHIN IGAKU, V43, P431 Picardi A, 2004, J PSYCHOSOM RES, V57, P219, DOI 10.1016/S0022-3999(03)00619-6 Woodbury-Smith MR, 2005, J AUTISM DEV DISORD, V35, P331, DOI 10.1007/s10803-005-3300-7 NR 14 TC 7 Z9 7 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1323-1316 J9 PSYCHIAT CLIN NEUROS JI Psychiatry Clin. Neurosci. PD JUN PY 2006 VL 60 IS 3 BP 373 EP 378 DI 10.1111/j.1440-1819.2006.01516.x PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 042GB UT WOS:000237514800017 PM 16732756 ER PT J AU Palmen, SJMC Durston, S Nederveen, H van Engeland, H AF Palmen, Saskia J. M. C. Durston, Sarah Nederveen, Hilde van Engeland, Herman TI No evidence for preferential involvement of medial temporal lobe structures in high-functioning autism SO PSYCHOLOGICAL MEDICINE LA English DT Article ID SPECTRUM DISORDER; HUMAN HIPPOCAMPUS; SOCIAL-BEHAVIOR; MRI VOLUMES; AMYGDALA; BRAIN; NEUROANATOMY; CHILDREN; NAIVE; AREA AB Background. Autism is a neurodevelopmental disorder associated with slight increases in brain volume. There has been some suggestion that medial temporal lobe structures may be preferentially involved in this disorder, although results have not always been consistent. Here, we investigate amygdala and hippocampus volumes in medication-naive subjects with high-functioning autism. Method. Whole-brain magnetic resonance imaging scans were acquired from 42 patients and 42 closely matched, healthy control subjects. Results. Amygdala volume did not differ significantly between patients and controls. A significant increase in hippocampal volume was proportional to an increase in overall brain volume. Conclusions. These results argue against preferential involvement of medial temporal lobe structures in autism, at least in high-functioning medication-naive individuals. C1 Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, Rudolf Magnus Inst Neurosci, NL-3584 CX Utrecht, Netherlands. RP Palmen, SJMC (reprint author), Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, Rudolf Magnus Inst Neurosci, HP A01 468, NL-3584 CX Utrecht, Netherlands. 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Med. PD JUN PY 2006 VL 36 IS 6 BP 827 EP 834 DI 10.1017/S0033291706007215 PG 8 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 052NC UT WOS:000238239400010 PM 16512972 ER PT J AU Ashwin, C Wheelwright, S Baron-Cohen, S AF Ashwin, C Wheelwright, S Baron-Cohen, S TI Attention bias to faces in Asperger Syndrome: a pictorial emotion Stroop study SO PSYCHOLOGICAL MEDICINE LA English DT Article ID PRECONSCIOUS SELECTIVE ATTENTION; FUNCTIONING AUTISM; CHILDREN; ANXIETY; STIMULI; THREAT; RECOGNITION; DISORDERS; QUOTIENT; ADULTS AB Background. Emotional Stroop tasks have shown attention biases of clinical populations towards stimuli related to their condition. Asperger Syndrome (AS) is a neuropsychiatric condition with social and communication deficits, repetitive behaviours and narrow interests. Social deficits are particularly striking, including difficulties in understanding others. Method. We investigated colour-naming latencies of adults with and without AS to name colours of pictures containing angry facial expressions, neutral expressions or non-social objects. We tested three hypotheses: whether (1) controls show longer colour-naming latencies for angry versus neutral facial expressions with male actors, (2) people with AS show differential latencies across picture types, and (3) differential response latencies persist when photographs contain females. Results. Controls had longer latencies to pictures of male faces with angry compared to neutral expressions. The AS group did not show longer latencies to angry versus neutral expressions in male faces, instead showing slower latencies to pictures containing any facial expression compared to objects. When pictures contained females, controls no longer showed longer latencies for angry versus neutral expressions. However, the AS group still showed longer latencies to all facial picture types, compared to objects, providing further evidence that faces produce interference effects for this clinical group. Conclusions. The pictorial emotional Stroop paradigm reveals normal attention biases towards threatening emotional faces. The AS group showed Stroop interference effects to all facial stimuli regardless of expression or sex, suggesting that faces cause disproportionate interference in AS. C1 Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 2AH, England. RP Ashwin, C (reprint author), Univ Cambridge, Autism Res Ctr, Dept Psychiat, Douglas House,18b Trumpington Rd, Cambridge CB2 2AH, England. 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PD JUN PY 2006 VL 36 IS 6 BP 835 EP 843 DI 10.1017/S0033291706007203 PG 9 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 052NC UT WOS:000238239400011 PM 16512970 ER PT J AU Bayliss, AP Tipper, SP AF Bayliss, AP Tipper, SP TI Predictive gaze cues and personality judgments - Should eye trust you? SO PSYCHOLOGICAL SCIENCE LA English DT Article ID VISUAL-ATTENTION; AUTISM-SPECTRUM; PERCEPTION; DIRECTION; FACE; CONTEXT; MEMORY; SHIFTS AB Although following another person's gaze is essential in fluent social interactions, the reflexive nature of this gaze-cuing effect means that gaze can be used to deceive. In a gaze-cuing procedure, participants were presented with several faces that looked to the left or right. Some faces always looked to the target (predictive-valid), some never looked to the target (predictive-invalid), and others looked toward and away from the target in equal proportions (nonpredictive). The standard gaze-cuing effects appeared to be unaffected by these contingencies. Nevertheless, participants tended to choose the predictive-valid faces as appearing more trustworthy than the predictive-invalid faces. This effect was negatively related to scores on a scale assessing autistic-like traits. Further, we present tentative evidence that the "deceptive" faces were encoded more strongly in memory than the "cooperative" faces. These data demonstrate the important interactions among attention, gaze perception, facial identity recognition, and personality judgments. C1 Univ Wales, Sch Psychol, Ctr Cognit Neurosci, Bangor LL57 2AS, Gwynedd, Wales. RP Bayliss, AP (reprint author), Univ Wales, Sch Psychol, Ctr Cognit Neurosci, Brigantia Bldg,Penrallt Rd, Bangor LL57 2AS, Gwynedd, Wales. 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Sci. PD JUN PY 2006 VL 17 IS 6 BP 514 EP 520 DI 10.1111/j.1467-9280.2006.01737.x PG 7 WC Psychology, Multidisciplinary SC Psychology GA 050CC UT WOS:000238064100011 PM 16771802 ER PT J AU [Anonymous] AF [Anonymous] TI Feedback help for people with autism SO PSYCHOLOGIST LA English DT News Item NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD JUN PY 2006 VL 19 IS 6 BP 335 EP 335 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 051GZ UT WOS:000238150900005 ER PT J AU Cosden, M Koegel, LK Koegel, RL Greenwell, A Klein, E AF Cosden, Merith Koegel, Lynn Kern Koegel, Robert L. Greenwell, Ashley Klein, Eileen TI Strength-based assessment for children with autism spectrum disorders SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article ID QUALITY-OF-LIFE; POSITIVE PSYCHOLOGY; SELF-DETERMINATION; DEVELOPMENTAL-DISABILITIES; FUNCTIONAL ASSESSMENT; BEHAVIORAL TREATMENT; INTERVENTION; SUPPORTS; STUDENTS; INDIVIDUALS AB Despite improvements in interventions for children with autism, assessments tend to focus on their social, cognitive, and behavioral deficits, without similar systematic examination of their strengths. Strength-based assessment (SBA), which has been used in work with children with milder behavioral disorders, may also have value for individuals who have autism. Although not supplanting usual assessment procedures, SBA provides a method for identifying personal, familial, and broader contextual strengths. Research outside the area of autism has found that SBA can be a useful addition to assessment protocols because it provides specific information on assets that can be incorporated into interventions. Further, SBA has the potential to affect the attitudes and beliefs of parents and educators involved in the assessment, creating greater hope about the ability of the child to function well and contributing to a stronger bond between the assessor, the child, and their family. This article describes ways in which SBA can be added to typical assessment protocols for children with autism. Examples are provided on how to identify and utilize strengths that can be used for planning interventions and for building more effective working relationships between clinicians and children with autism and their families. Areas for future research are also discussed. C1 Univ Calif Santa Barbara, Gervitz Grad Sch Educ, Sch Psychol, Santa Barbara, CA 93106 USA. 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Pract. Pers. Sev. Disabil. PD SUM PY 2006 VL 31 IS 2 BP 134 EP 143 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 075UH UT WOS:000239910200006 ER PT J AU Cosbey, JE Johnston, S AF Cosbey, Joanna Evans Johnston, Susan TI Using a single-switch voice output communication aid to increase social access for children with severe disabilities in inclusive classrooms SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article ID PROFOUND MULTIPLE DISABILITIES; YOUNG-CHILDREN; DEVELOPMENTAL DELAYS; PRESCHOOL-CHILDREN; STUDENTS; AUTISM; SKILLS; PLAY; INTERVENTIONS; INITIATIONS AB Three young children with severe, multiple disabilities were taught to utilize a voice output communication aid (VOCA) to request access to preferred items and/or peers during play activities. Acquisition of VOCA use resulted from a naturalistic intervention strategy that consisted of creating communication opportunities, prompting the participant to engage in the target behavior via a full physical prompt, and facilitating access to natural consequences for appropriate participant responses. Intervention occurred in the context of naturally occurring free-choice activities in inclusive classrooms. Results showed that the intervention strategy was effective in teaching all three participants to use a VOCA to request access to items and/or peers. The peers generally responded to the participants with either positive or neutral responses. Survey data on the acceptability of the intervention to classroom staff are also discussed. C1 Univ Utah, Dept Special Educ, Salt Lake City, UT 84112 USA. RP Cosbey, JE (reprint author), Univ Utah, Dept Special Educ, 1705 Campus Ctr Dr,Room 221, Salt Lake City, UT 84112 USA. 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Increased vulnerability to psychiatric disorders characterized by difficulties in social interactions, such as schizophrenia and autism, has been reported for this population. The reported social difficulties in 47,XXY men may arise as a consequence of impairments in the processing of social and emotional information. The present study is the first investigation of social-emotional information processing in this X chromosomal disorder. 32 Klinefelter men and 26 men from the general population, with the groups matched for age, educational level and I.Q., participated in the study. Several tasks were included, reflecting aspects of social-emotional information processing on levels of perception, experience and expression: labeling of facial expressions of emotion, emotion-cognition interactions in decision making and emotion regulation, that refers to subjective experience and identification of emotional arousal as well as verbal expression of emotions. A discrepancy between cognitive appraisal of emotions and emotional arousal was observed in Klinefelter syndrome. Taken together, Klinefelter men seem less accurate in perception of socio-emotional cues such as angry facial expressions, they are less able to identify and verbalize their emotions, but experience increased levels of emotional arousal, in comparison to the general population. Besides describing the social-emotional phenotype of this X chromosomal disorder, the present data may prove to be an important contribution to the development of more general models describing pathways to neuropsychiattic disorders characterized by social cognitive disturbances. (c) 2006 Elsevier B.V All rights reserved. C1 Univ Utrecht, Helmholtz Inst, Dept Expt Psychol, NL-3508 TC Utrecht, Netherlands. Univ Utrecht, Med Ctr, Rudolf Magnus Inst Neurosci, Dept Psychiat, NL-3584 CX Utrecht, Netherlands. Leiden Univ, Dept Clin Child & Adolescent Studies, NL-2333 AK Leiden, Netherlands. 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Res. PD JUN PY 2006 VL 84 IS 2-3 BP 194 EP 203 DI 10.1016/j.schres.2006.02.020 PG 10 WC Psychiatry SC Psychiatry GA 051KR UT WOS:000238160500002 PM 16603340 ER PT J AU Golan, O Baron-Cohen, S Hill, JJ Golan, Y AF Golan, Ofer Baron-Cohen, Simon Hill, Jacqueline J. Golan, Yael TI The "Reading the Mind in Films" Task: Complex emotion recognition in adults with and without autism spectrum conditions SO SOCIAL NEUROSCIENCE LA English DT Article ID HIGH-FUNCTIONING AUTISM; CEREBRAL-BLOOD-FLOW; FUSIFORM FACE AREA; ASPERGER-SYNDROME; FACIAL EXPRESSIONS; DEVELOPING-CHILDREN; SOCIAL COGNITION; EMPATHY QUOTIENT; BRAIN; FMRI AB Background: Individuals with autism spectrum conditions (ASC) have difficulties recognizing mental states in others. Most research has focused on recognition of basic emotions from faces and voices separately. This study reports the results of a new task, assessing recognition of complex emotions and mental states from social scenes taken from feature films. The film format arguably is more challenging and ecologically closer to real social situations. Sample and method: A group of adults with ASC (n = 22) were compared to a group of matched controls from the general population (n = 22). Participants were tested individually. Results: Overall, individuals with ASC performed significantly lower than controls. There was a positive correlation between verbal IQ and task scores. Using task scores, more than 90% of the participants were correctly allocated to their group. Item analysis showed that the errors individuals with ASC make when judging socioemotional information are subtle. Conclusions: This new test of complex emotion and mental state recognition reveals that adults with ASC have residual difficulties in this aspect of empathy. The use of language-based compensatory strategies for emotion recognition is discussed. 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PD JUN PY 2006 VL 1 IS 2 BP 111 EP 123 DI 10.1080/17470910600980986 PG 13 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QW UT WOS:000252245000004 PM 18633780 ER PT J AU Chapman, E Baron-Cohen, S Auyeung, B Knickmeyer, R Taylor, K Hackett, G AF Chapman, Emma Baron-Cohen, Simon Auyeung, Bonnie Knickmeyer, Rebecca Taylor, Kevin Hackett, Gerald TI Fetal testosterone and empathy: Evidence from the Empathy Quotient (EQ) and the "Reading the Mind in the Eyes" Test SO SOCIAL NEUROSCIENCE LA English DT Article ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; CONGENITAL ADRENAL-HYPERPLASIA; CENTRAL NERVOUS-SYSTEM; ASPERGER-SYNDROME; HUMAN BRAIN; SYSTEMATIZING QUOTIENT; PRENATAL TESTOSTERONE; SPECTRUM DISORDER; SPATIAL ABILITY AB Empathy involves an understanding of what others are thinking and feeling, and enables us to interact in the social world. According to the Empathizing-Systemizing (E-S) theory, females on average have a stronger drive to empathize than males. This sex difference may in part reflect developmental differences in brain structure and function, which are themselves under the influence of fetal testosterone (fT) Previous studies have found that fT is inversely correlated with social behaviors such as eye contact in infancy, peer relationships in preschoolers, and mentalistic interpretation of animate motion. Male fetuses are exposed to higher levels of testosterone than are female fetuses. The present study investigates empathizing in children, as a function of amniotic measures of fT. One hundred ninety-three mothers of children (100 males, 93 females) aged 6-8 years of age completed children's versions of the Empathy Quotient (EQ-C), and the children themselves were tested on "Reading the Mind in the Eyes" Task (Eyes-C). All mothers had had amniocentesis during the 2nd trimester of pregnancy. There was a significant negative correlation between fT and scores on both measures. While empathy may be influenced by post-natal experience, these results suggest that pre-natal biology also plays an important role, mediated by androgen effects in the brain. These results also have implications for the causes of disabilities involving empathy, such as autism spectrum conditions, and may explain the increased rate of such conditions among males. C1 [Chapman, Emma; Baron-Cohen, Simon; Auyeung, Bonnie; Knickmeyer, Rebecca] Univ Cambridge, Austim Res Ctr, Cambridge CB2 2AH, England. [Knickmeyer, Rebecca] Univ N Carolina, Chapel Hill, NC USA. [Taylor, Kevin; Hackett, Gerald] Addenbrookes Hosp, Cambridge, England. RP Chapman, E (reprint author), Univ Cambridge, Austim Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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Neurosci. PD JUN PY 2006 VL 1 IS 2 BP 135 EP 148 DI 10.1080/17470910600992239 PG 14 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 249QW UT WOS:000252245000006 PM 18633782 ER PT J AU Wetherby, AM Woods, JJ AF Wetherby, Amy M. Woods, Juliann J. TI Early social interaction project for children with autism spectrum disorders beginning in the second year of life: A preliminary study SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; EARLY INTERVENTION; EARLY IDENTIFICATION; JOINT ATTENTION; COMMUNICATION; LANGUAGE; REGRESSION; AGE; RELIABILITY AB The Early Social Interaction (ESI) Project (Woods & Wetherby, 2003) was designed to apply the recommendations of the National Research Council (2001) to toddlers with autism spectrum disorders (ASD) by using a parent-implemented intervention that (a) embeds naturalistic teaching strategies in everyday routines and (b) is compatible with the mandate of the Individuals with Disabilities Education Improvement Act (IDEIA) of 2004, Part C. This quasi-experimental study is a preliminary effort by the authors to evaluate the effects of ESI on the social communication outcomes for a group of 17 children with ASD who entered ESI at age 2 years. The results indicated significant improvement on 11 of 13 social communication measures. The researchers compared the ESI group with a contrast group of 18 children with ASD who entered early intervention at age 3 years. The contrast group's results were comparable to those of the ESI postintervention group on communicative means and play, but the contrast group as a whole demonstrated significantly poorer performance on all other social communication measures. These findings offer promise for the use of parent-implemented interventions in promoting social communication for toddlers with ASD. C1 Florida State Univ, Dept Commun Disorders, Tallahassee, FL 32306 USA. RP Wetherby, AM (reprint author), Florida State Univ, Dept Commun Disorders, RRC 017, Tallahassee, FL 32306 USA. 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S., 2001, EARLY CHILDHOOD INCL, P337 Tager-Flusberg H., 2005, HDB AUTISM PERVASIVE, P335 Walsh S., 2000, YOUNG EXCEPTIONAL CH, V2, P3 Wetherby A., 2003, COMMUNICATION SYMBOL WETHERBY A, IN PRESS J AUTISM DE Wetherby AM, 1998, AM J SPEECH-LANG PAT, V7, P79 Wetherby AM, 2002, J SPEECH LANG HEAR R, V45, P1202, DOI 10.1044/1092-4388(2002/097) Wetherby AM, 2002, COMMUNICATION SYMBOL Wetherby AM, 2004, J AUTISM DEV DISORD, V34, P473, DOI 10.1007/s10803-004-2544-y Wetherby AM, 2003, INFANT YOUNG CHILD, V16, P161 Whalen C, 2003, J CHILD PSYCHOL PSYC, V44, P456, DOI 10.1111/1469-7610.00135 Woods J, 2004, J EARLY INTERVENTION, V26, P175, DOI 10.1177/105381510402600302 Woods JJ, 2003, LANG SPEECH HEAR SER, V34, P180, DOI 10.1044/0161-1461(2003/015) NR 63 TC 37 Z9 37 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0271-1214 J9 TOP EARLY CHILD SPEC JI Top. Early Child. Spec. Educ. PD SUM PY 2006 VL 26 IS 2 BP 67 EP 82 DI 10.1177/02711214060260020201 PG 16 WC Education, Special SC Education & Educational Research GA 079NK UT WOS:000240183400001 ER PT J AU Hine, JF Wolery, M AF Hine, Jeffrey F. Wolery, Mark TI Using point-of-view video modeling to teach play to preschoolers with autism SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID PERSPECTIVE-TAKING; PURCHASING SKILLS; SYMBOLIC PLAY; CHILDREN; SELF; REINFORCEMENT; ACQUISITION; DISORDER AB This study evaluated the effectiveness of point-of-view video modeling in teaching selected toy-play skills to two preschoolers with autism. This type of modeling involved the experimenters carrying or holding the video camera at eye level v e child's perspective) and without recording models (persons]) to show environment as a child would see it when he or she was performing the targeted skills. The researchers used a multiple-probe design across two children and two behaviors to evaluate the effect of the point-of-view modeling on the children's acquisition and maintenance of play actions. They used generalization probes to assess the degree to which the participants used the new skills across novel toys and during classroom activities. The results indicated that point-of-view modeling was an effective tool for teaching toy-play actions to preschoolers with autism. The authors discuss the extension of current video modeling research and implications for home and school interventions. C1 Vanderbilt Univ, Peabody Coll, Nashville, TN 37240 USA. RP Hine, JF (reprint author), 27730 Lake Jem Rd, Mt Dora, FL 32757 USA. EM jeffhine@hotmail.com CR ALCANTARA PR, 1994, EXCEPT CHILDREN, V61, P40 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BANDURA A, 1965, J PERS SOC PSYCHOL, V1, P589, DOI 10.1037/h0022070 BUGGEY T, 1999, J POSITIVE BEHAV INT, V4, P205 CHARLOP MH, 1983, J ABNORM CHILD PSYCH, V11, P355, DOI 10.1007/BF00914244 CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 Charlop-Christy MH, 2000, J AUTISM DEV DISORD, V30, P537, DOI 10.1023/A:1005635326276 Charlop-Christy MH, 2003, J POSIT BEHAV INTERV, V5, P12, DOI 10.1177/10983007030050010101 D'Ateno P, 2003, J POSIT BEHAV INTERV, V5, P5, DOI 10.1177/10983007030050010801 Dawson G., 1997, EFFECTIVENESS EARLY, P307 HARING TG, 1987, J APPL BEHAV ANAL, V20, P89, DOI 10.1901/jaba.1987.20-89 Hepting NH, 1996, TOP EARLY CHILD SPEC, V16, P407 HORNER RD, 1978, J APPL BEHAV ANAL, V11, P189, DOI 10.1901/jaba.1978.11-189 INGERSOLL B, 2003, J AUTISM DEV DISORD, V6, P673 Jarrold C, 2003, AUTISM, V7, P379, DOI 10.1177/1362361303007004004 JARROLD C, 1993, J AUTISM DEV DISORD, V23, P281, DOI 10.1007/BF01046221 Jordan R., 1997, AUTISM LEARNING GUID Kinney EM, 2003, J POSIT BEHAV INTERV, V5, P22, DOI 10.1177/10983007030050010301 LeBlanc LA, 2003, J APPL BEHAV ANAL, V36, P253, DOI 10.1901/jaba.2003.36-253 Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 Nikopoulos CK, 2004, J APPL BEHAV ANAL, V37, P93, DOI 10.1901/jaba.2004.37-93 Pierce-Jordan S, 2005, TOP EARLY CHILD SPEC, V25, P34, DOI 10.1177/02711214050250010401 Schreibman L., 2000, J POSIT BEHAV INTERV, V2, P3, DOI 10.1177/109830070000200102 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 Shipley-Benamou R, 2002, J POSIT BEHAV INTERV, V4, P165 Stahmer AC, 2003, AUTISM, V7, P401, DOI 10.1177/1362361303007004006 Stone WL, 1997, J ABNORM CHILD PSYCH, V25, P475, DOI 10.1023/A:1022685731726 Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 Van Berckelaer-Onnes IA, 2003, AUTISM, V7, P415, DOI 10.1177/1362361303007004007 Wert BY, 2003, J POSIT BEHAV INTERV, V5, P30, DOI 10.1177/10983007030050010501 Zihni F., 2005, AZ METHOD USE VIDEO NR 32 TC 54 Z9 54 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0271-1214 J9 TOP EARLY CHILD SPEC JI Top. Early Child. Spec. Educ. PD SUM PY 2006 VL 26 IS 2 BP 83 EP 93 DI 10.1177/02711214060260020301 PG 11 WC Education, Special SC Education & Educational Research GA 079NK UT WOS:000240183400002 ER PT J AU Boulware, GL Schwartz, IS Sandall, SR McBride, BJ AF Boulware, Gusty-Lee Schwartz, Ilene S. Sandall, Susan R. McBride, Bonnie J. TI Project DATA for toddlers: yAn inclusive approach to very young children with autism spectrum disorder SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID COMMUNICATION; INTERVENTION; DIAGNOSIS; BEHAVIOR; OUTCOMES; SCHOOL AB Because more children under the age of 3 years are being diagnosed with autistic spectrum disorder (ASD), early interventionists face the challenge of identifying B appropriate programs to meet the unique needs of very young children with ASD and their families. Project DATA (Developmentally Appropriate Treatment for Autism) for Toddlers is an inclusive early intervention program for children between I year and 3 years old who have been diagnosed with ASD and is based on an existing program for preschoolers with ASD at the University of Washington. Project DATA for Toddlers uses the effective preschool model and makes modifications to meet the unique developmental needs of toddlers. In this article, the authors describe the components of Project DATA for Toddlers and present preliminary findings, specifically, child outcome data from the areas of cognition, communication, self-regulation, functional skills, and elementary school placement. They also discuss the implications for early intervention service delivery programs. C1 Univ Washington, Expt Educ Unit, Seattle, WA 98195 USA. RP Boulware, GL (reprint author), Univ Washington, Expt Educ Unit, Box 357925, Seattle, WA 98195 USA. EM bouleware@u.washington.edu CR Bagnato SJ, 1999, INFANT YOUNG CHILD, V12, P98 Bayley N, 1993, BAYLEY SCALES INFANT Bondy Andrew S., 1994, PRESCHOOL ED PROGRAM, P37 BOULWARE G, 2000, C RES INN EARL INT S Boulware G., 1999, YOUNG EXCEPTIONAL CH, V3, P21, DOI 10.1177/109625069900300103 Bricker D., 1993, ASSESSMENT EVALUATIO Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 Dawson G., 1997, EFFECTIVENESS EARLY, P307 Filipek PA, 2000, NEUROLOGY, V55, P468 Fox L, 2000, COMM LANG INTERVEN, V9, P307 Frost L., 2002, PICTURE EXCHANGE COM, V2nd Gomez C. R., 2005, FOCUS AUTISM OTHER D, V20, P106, DOI [10.1177/10883576050200020101, DOI 10.1177/10883576050200020101] HANDLEMAN JS, 1994, PRESCHOOL ED PROGRAM, P71 HARRIS SL, 1994, PRESCHOOL ED PROGRAM Hepting NH, 1996, J EARLY INTERVENTION, V20, P249 Kelly J., 2000, HDB EARLY CHILDHOOD, P258 Kern L, 1998, ANTECEDENT CONTROL, P289 Kochanek TT, 1998, J EARLY INTERVENTION, V21, P217 KOEGEL RL, 1977, J APPL BEHAV ANAL, V10, P197, DOI 10.1901/jaba.1977.10-197 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Lucyshyn J. M., 2002, FAMILIES POSITIVE BE McBride BJ, 2003, TOP EARLY CHILD SPEC, V23, P5, DOI 10.1177/027112140302300102 MCCOLLUM JA, 1994, INFANTS YOUNG CHILDR, V6, P26 McGee GG, 1999, J ASSOC PERS SEVERE, V24, P133, DOI 10.2511/rpsd.24.3.133 McLean M. E., 2005, DEC RECOMMENDED PRAC National Research Council Committee on Interventions for Children with Autism, 2001, ED CHILDR AUT Neisworth JT, 1999, TABS MANUAL TEMPERAM Prizant BM, 2003, INFANT YOUNG CHILD, V16, P296 Sandall S. R., 2002, BUILDING BLOCKS TEAC SCHWARTZ IS, 1998, YOUNG EXCEPTIONAL CH, V2, P19 Schwartz IS, 2004, TOP EARLY CHILD SPEC, V24, P156, DOI 10.1177/02711214040240030301 Stahmer AC, 2004, J POSIT BEHAV INTERV, V6, P67, DOI 10.1177/10983007040060020201 Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 Wetherby AM, 1992, COMMUNICATION SYMBOL Wolery M., 1992, TEACHING STUDENTS MO WOLERY M, 1983, EXCEPT CHILDREN, V50, P167 Woods J, 2004, J EARLY INTERVENTION, V26, P175, DOI 10.1177/105381510402600302 NR 37 TC 7 Z9 7 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0271-1214 J9 TOP EARLY CHILD SPEC JI Top. Early Child. Spec. Educ. PD SUM PY 2006 VL 26 IS 2 BP 94 EP 105 DI 10.1177/02711214060260020401 PG 12 WC Education, Special SC Education & Educational Research GA 079NK UT WOS:000240183400003 ER PT J AU Tsao, LL Odom, SL AF Tsao, Ling-Ling Odom, Samuel L. TI Sibling-mediated social interaction intervention for young children with autism SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID JOINT ATTENTION; BEHAVIOR-MODIFICATION; PRESCHOOLERS; SKILLS; DISABILITIES; INITIATIONS; STRATEGY; PROGRAM; HOME AB In the present study, the authors investigated the effectiveness of a sibling-mediated intervention in supporting the social behaviors of young children with autism. They l used a multiple-baseline design across four sibling dyads to examine the effectiveness of the intervention. The researchers taught the typically developing siblings ways to socially engage their brothers with autism, which resulted in strong and positive changes in joint attention and modest changes in social behavior for the latter. Social validity ratings by observers who were naive to the study parameters documented the social importance of the intervention effects for three of the four children; however, the results did not provide strong evidence for generalization of increased social interactions to different settings. The authors also discuss the practical implications of their findings. C1 Univ Wisconsin, Coll Educ & Human Serv, Oshkosh, WI 54901 USA. Indiana Univ, Bloomington, IN 47405 USA. RP Tsao, LL (reprint author), Univ Wisconsin, Coll Educ & Human Serv, 800 Algoma Blvd, Oshkosh, WI 54901 USA. EM tsool@uwosh.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Brown WH, 2001, TOP EARLY CHILD SPEC, V21, P162, DOI 10.1177/027112140102100304 Caldwell C. 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R., 1980, EXCEPTIONAL TEACHING WOLF MM, 1978, J APPL BEHAV ANAL, V11, P203, DOI 10.1901/jaba.1978.11-203 Woods JJ, 2003, LANG SPEECH HEAR SER, V34, P180, DOI 10.1044/0161-1461(2003/015) NR 48 TC 25 Z9 25 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0271-1214 J9 TOP EARLY CHILD SPEC JI Top. Early Child. Spec. Educ. PD SUM PY 2006 VL 26 IS 2 BP 106 EP 123 DI 10.1177/02711214060260020101 PG 18 WC Education, Special SC Education & Educational Research GA 079NK UT WOS:000240183400004 ER PT J AU Behrmann, M Thomas, C Humphreys, K AF Behrmann, Marlene Thomas, Cibu Humphreys, Kate TI Seeing it differently: visual processing in autism SO TRENDS IN COGNITIVE SCIENCES LA English DT Review ID HIGH-FUNCTIONING AUTISM; FUSIFORM FACE AREA; SOCIAL DEVELOPMENTAL DISORDERS; WEAK CENTRAL COHERENCE; SPECTRUM DISORDER; EYE-GAZE; ASPERGER-SYNDROME; LOCAL PRECEDENCE; FACIAL IDENTITY; YOUNG-CHILDREN AB Several recent behavioral and neuroimaging studies have documented an impairment in face processing in individuals with Autism Spectrum Disorder (ASD). It remains unknown, however, what underlying mechanism gives rise to this face processing difficulty. One theory suggests that the difficulty derives from a pervasive problem in social interaction and/or motivation. An alternative view proposes that the face-processing problem is not entirely social in nature and that a visual perceptual impairment might also contribute. The focus of this review is on this latter, perceptual perspective, documenting the psychological and neural alterations that might account for the face processing impairment. The available evidence suggests that perceptual alterations are present in ASD, independent of social function. C1 Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, Ctr Neural Basis Cognit, Pittsburgh, PA 15213 USA. RP Behrmann, M (reprint author), Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. 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SCI. PD JUN PY 2006 VL 10 IS 6 BP 258 EP 264 DI 10.1016/j.tics.2006.05.001 PG 7 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 060UO UT WOS:000238827300007 PM 16713326 ER PT J AU Burns, J AF Burns, Jonathan TI The social brain hypothesis of schizophrenia SO WORLD PSYCHIATRY LA English DT Article DE Schizophrenia; social brain; autism; evolution; connectivity ID SHARED MANIFOLD HYPOTHESIS; FACE RECOGNITION; MIRROR NEURONS; FACIAL AFFECT; NEGATIVE-SYMPTOMS; MIND; COGNITION; SYMPTOMATOLOGY; DEFICIT; INTERSUBJECTIVITY AB The social brain hypothesis is a useful heuristic for understanding schizophrenia. It focuses attention on the core Bleulerian concept of autistic alienation and is consistent with well-replicated findings of social brain dysfunction in schizophrenia, as well as contemporary theories of human cognitive and brain evolution. The contributions of Heidegger, Merleau-Ponty and Wittgenstein allow us to arrive at a new "philosophy of interpersonal relatedness", which better reflects the "embodied mind" and signifies the end of Cartesian dualistic thinking. In this paper I review the evolution, development and neurobiology of the social brain - the anatomical and functional substrate for adaptive social behaviour and cognition. Functional imaging identifies fronto-temporal and fronto-parietal cortical networks as comprising the social brain, while the discovery of "mirror neurons" provides an understanding of social cognition at a cellular level. Patients with schizophrenia display abnormalities in a wide range of social cognition tasks such as emotion recognition, theory of mind and affective responsiveness. Furthermore, recent research indicates that schizophrenia is a disorder of functional and structural connectivity of social brain networks. These findings lend support to the claim that schizophrenia represents a costly by-product of social brain evolution in Homo sapiens. Individuals with this disorder find themselves seriously disadvantaged in the social arena and vulnerable to the stresses of their complex social environments. This state of "disembodiment" and interpersonal alienation is the core phenomenon of schizophrenia and the root cause of intolerable suffering in the lives of those affected. C1 Univ KwaZulu Natal, Nelson Mandela Sch Med, Dept Psychiat, ZA-4000 Durban, South Africa. RP Burns, J (reprint author), Univ KwaZulu Natal, Nelson Mandela Sch Med, Dept Psychiat, ZA-4000 Durban, South Africa. 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Quackenbush, John TI Gene expression profiling of lymphoblastoid cell lines from monozygotic twins discordant in severity of autism reveals differential regulation of neurologically relevant genes SO BMC GENOMICS LA English DT Article ID TUBEROUS SCLEROSIS GENE; BIPOLAR DISORDER; CANDIDATE GENES; NITRIC-OXIDE; ARGININOSUCCINATE SYNTHETASE; PSYCHIATRIC-DISORDERS; DNA MICROARRAYS; MESSENGER-RNA; CHROMOSOME 7Q; LINKAGE AB Background: The autism spectrum encompasses a set of complex multigenic developmental disorders that severely impact the development of language, non-verbal communication, and social skills, and are associated with odd, stereotyped, repetitive behavior and restricted interests. To date, diagnosis of these neurologically based disorders relies predominantly upon behavioral observations often prompted by delayed speech or aberrant behavior, and there are no known genes that can serve as definitive biomarkers for the disorders. Results: Here we demonstrate, for the first time, that lymphoblastoid cell lines from monozygotic twins discordant with respect to severity of autism and/or language impairment exhibit differential gene expression patterns on DNA microarrays. Furthermore, we show that genes important to the development, structure, and/or function of the nervous system are among the most differentially expressed genes, and that many of these genes map closely in silico to chromosomal regions containing previously reported autism candidate genes or quantitative trait loci. Conclusion: Our results provide evidence that novel candidate genes for autism may be differentially expressed in lymphoid cell lines from individuals with autism spectrum disorders. This finding further suggests the possibility of developing a molecular screen for autism based on expressed biomarkers in peripheral blood lymphocytes, an easily accessible tissue. 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Multidisciplinary Sciences SC Science & Technology - Other Topics GA 043IB UT WOS:000237593200011 PM 16710386 ER PT J AU Paylor, R Glaser, B Mupo, A Ataliotis, P Spencer, C Sobotka, A Sparks, C Choi, CH Oghalai, J Curran, S Murphy, KC Monks, S Williams, N O'Donovan, MC Owen, MJ Scambler, PJ Lindsay, E AF Paylor, R Glaser, B Mupo, A Ataliotis, P Spencer, C Sobotka, A Sparks, C Choi, CH Oghalai, J Curran, S Murphy, KC Monks, S Williams, N O'Donovan, MC Owen, MJ Scambler, PJ Lindsay, E TI Tbx1 haploinsufficiency is linked to behavioral disorders in mice and humans: Implications for 22q11 deletion syndrome SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE mouse model; psychiatric disease; DiGeorge syndrome; sensorimotor gating ID DIGEORGE-SYNDROME REGION; CARDIO-FACIAL/DIGEORGE-SYNDROME; HIGH-FUNCTIONING AUTISM; CARDIOVASCULAR DEFECTS; PREPULSE INHIBITION; CHROMOSOMAL DELETIONS; SYNDROME PHENOTYPE; ASPERGER-SYNDROME; FACIAL SYNDROME; SCHIZOPHRENIA AB About 35% of patients with 22q11 deletion syndrome (22q11DS), which includes DiGeorge and velocardiofacial syndromes, develops psychiatric disorders, mainly schizophrenia and bipolar disorder. We previously reported that mice carrying a multigene deletion (Df1) that models 22q11DS have reduced prepulse inhibition (PPI), a behavioral abnormality and schizophrenia endophenotype. Impaired PPI is associated with several psychiatric disorders, including those that occur in 22q11DS, and recently, reduced PPI was reported in children with 22q11DS. Here, we have mapped PPI deficits in a panel of mouse mutants that carry deletions that partially overlap with DO and have defined a PPI critical region encompassing four genes. We then used single-gene mutants to identify the causative genes. We show that PIPI deficits in Df1/+ mice are caused by haploinsufficiency of two genes, Tbx1 and Gnb1l. Mutation of either gene is sufficient to cause reduced PPI. Tbx1 is a transcription factor, the mutation of which is sufficient to cause most of the physical features of 22q11DS, but the gene had not been previously associated with the behavioral/psychiatric phenotype. A likely role for Tbx1 haploinsufficiency in psychiatric disease is further suggested by the identification of a family in which the phenotypic features of 22q11DS, including psychiatric disorders, segregate with an inactivating mutation of TBX1. One family member has Asperger syndrome, an autistic spectrum disorder that is associated with reduced PPI. Thus, Tbx1 and Gnb1I are strong candidates for psychiatric disease in 22q11DS patients and candidate susceptibility genes for psychiatric disease in the wider population. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA. Baylor Coll Med, Dept Pediat Cardiol, Houston, TX 77030 USA. Baylor Coll Med, Dept Otolaryngol, Houston, TX 77030 USA. Univ Cardiff Wales, Dept Med Psychol, Cardiff CF14 4XN, Wales. CEINGE Biotecnol Avanzate, I-80145 Naples, Italy. European Sch Mol Med, SEMM, I-80145 Naples, Italy. Inst Child Hlth, Mol Med Unit, London WC1N 1EH, England. 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Epidemiological studies have indicated that the risk of developing these disorders is enhanced by prenatal maternal infection, presumably as a result of neurodevelopmental defects triggered by cytokine-related inflammatory events. Here, we demonstrate that the effects of maternal immune challenge between middle and late gestation periods in mice are dissociable in terms of fetal brain cytokine responses to maternal inflammation and the pathological consequences in brain and behavior. Specifically, the relative expression of pro- and anti-inflammatory cytokines in the fetal brains in response to maternal immune challenge may be an important determinant among other developmental factors for the precise pathological profile emerging in later life. Thus, the middle and late gestation periods correspond to two windows with differing vulnerability to adult behavioral dysfunction, brain neuropathology in early adolescence, and of the acute cytokine responses in the fetal brain. 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Neurosci. PD MAY 3 PY 2006 VL 26 IS 18 BP 4752 EP 4762 DI 10.1523/JNEUROSCI.0099-06.2006 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 039AN UT WOS:000237271700004 PM 16672647 ER PT J AU Martchek, M Thevarkunnel, S Bauman, M Blatt, G Kemper, T AF Martchek, M Thevarkunnel, S Bauman, M Blatt, G Kemper, T TI Lack of evidence of neuropathology in the locus coeruleus in autism SO ACTA NEUROPATHOLOGICA LA English DT Letter ID NORADRENERGIC SYSTEM; NEURONS; BRAIN; NUMBER C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Kemper, T (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St, Boston, MA 02118 USA. EM tkemper@bu.edu CR ARANGO V, 1994, BRAIN RES, V650, P1, DOI 10.1016/0006-8993(94)90199-6 BAILEY A, 1998, BRAIN, V121, P899 BAKER KG, 1989, EXP BRAIN RES, V77, P257, DOI 10.1007/BF00274983 Berridge CW, 2003, BRAIN RES REV, V42, P33, DOI 10.1016/S0165-0173(03)00143-7 HASHIMOTO T, 1995, J AUTISM DEV DISORD, V25, P1, DOI 10.1007/BF02178163 Kemper TL, 1998, J NEUROPATH EXP NEUR, V57, P645, DOI 10.1097/00005072-199807000-00001 MANAYE KF, 1995, J COMP NEUROL, V358, P79, DOI 10.1002/cne.903580105 MORRISON JH, 1982, BRAIN RES BULL, V9, P309, DOI 10.1016/0361-9230(82)90144-7 MOUTON PR, 1994, J CHEM NEUROANAT, V7, P185, DOI 10.1016/0891-0618(94)90028-0 Nelson K. 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PD MAY PY 2006 VL 111 IS 5 BP 497 EP 499 DI 10.1007/s00401-006-0061-0 PG 3 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 039QY UT WOS:000237322900013 PM 16596425 ER PT J AU Sams, MJ Fortney, EV Willenbring, S AF Sams, MJ Fortney, EV Willenbring, S TI Occupational therapy incorporating animals for children with autism: A pilot investigation SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article ID INTERVENTIONS AB This investigation compared language use and social interaction-in children with autism receiving two forms of occupational therapy: occupational therapy using standard techniques, and occupational therapy incorporating animals. Twenty-two children between the ages of 7 and 13 received both forms of therapy in a school-based occupational therapy program for children with autism. Results suggest that the children demonstrated significantly greater use of language and significantly greater social interaction in sessions incorporating animals when compared to sessions using exclusively standard occupational therapy techniques. Findings are discussed in the context of recent research that has highlighted the importance of enhancing the motivation of children with autism to engage actively in therapeutic and learning processes. C1 Monas Ark, Troutville, VA 24175 USA. Cent State Hosp, Petersburg, VA USA. Dabney S Lancaster Community Coll, Clifton Forge, VA USA. RP Sams, MJ (reprint author), Monas Ark, 240 Old Mine Rd, Troutville, VA 24175 USA. EM evfortney@evfortney.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Ayers AJ, 1972, SENSORY INTEGRATION Baranek GT, 2002, J AUTISM DEV DISORD, V32, P397, DOI 10.1023/A:1020541906063 BARKER SB, 1998, J CHILD ADOL PSYCHOP, V10, P17 Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 Biery M. 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R., 1997, KINSHIP MASTERY BIOP Koegel LK, 2003, TOP LANG DISORD, V23, P134 KOEGEL LK, 2005, PSYCHOSOCIAL TREATME, P633 MAILLOUX Z, 2001, AUTISM COMPREHENSIVE, P101 MARTIN F, 2002, WESTERN J NURS RES, V26, P657 Melson Gail F., 1991, CHILDRENS ENV Q, V8, P55 MELSON GF, 1994, ANN M DELT SOC NEW Y Melson GF, 2003, AM BEHAV SCI, V47, P31, DOI 10.1177/0002764203255210 Merrick Joav, 2004, Int J Adolesc Med Health, V16, P75 Minshew N J, 1997, J Int Neuropsychol Soc, V3, P303 REDEFER LA, 1989, J AUTISM DEV DISORD, V19, P461, DOI 10.1007/BF02212943 Rogers SJ, 1998, MENT RETARD DEV D R, V4, P104 SCHUELKE ST, 1991, LATHAM LETT, V8, P14 Watling R, 1999, AM J OCCUP THER, V53, P498 NR 27 TC 19 Z9 19 PU AMER OCCUPATIONAL THERAPY ASSOC, INC PI BETHESDA PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA SN 0272-9490 J9 AM J OCCUP THER JI Am. J. Occup. Ther. PD MAY-JUN PY 2006 VL 60 IS 3 BP 268 EP 274 PG 7 WC Rehabilitation SC Rehabilitation GA 044MV UT WOS:000237677500005 PM 16776394 ER PT J AU Rabionet, R McCauley, JL Jaworski, JM Ashley-Koch, AE Martin, ER Sutcliffe, JS Haines, JL DeLong, GR Abramson, RK Wright, HH Cuccaro, ML Gilbert, JR Pericak-Vance, MA AF Rabionet, R McCauley, JL Jaworski, JM Ashley-Koch, AE Martin, ER Sutcliffe, JS Haines, JL DeLong, GR Abramson, RK Wright, HH Cuccaro, ML Gilbert, JR Pericak-Vance, MA TI Lack of association between autism and SLC25A12 SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID LINKAGE; CHROMOSOME-2; GENES AB Objective: Autism has a strong, complex genetic component, most likely involving several genes. Multiple genomic screens have shown evidence suggesting linkage to chromosome 2q31-q33, which includes the SLC25A12 gene. Recently, an association between autism risk and two single nucleotide polymorphisms (SNPs) in SLC25A12 was reported. This study aimed to test for association in SLC25A12 in an independent data set of 327 families with autistic offspring. Method: The authors analyzed two SNPs that were significant in the previous study group, as well as seven additional SNPs within the gene. Association analyses for individual SNPs as well as haplotypes were performed. Results: There was no evidence of an association between SLC25A12 and autism. Conclusions: These results suggest that SLC25A12 is not a major contributor to autism risk in these families. C1 Duke Univ, Med Ctr, Dept Med, Ctr Human Genet, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Med, Div Pediat, Durham, NC 27710 USA. Vanderbilt Univ, Med Ctr, Ctr Human Genet Res, Dept Mol Physiol & Biophys, Nashville, TN USA. Univ S Carolina, WS Hall Psychiat Inst, Columbia, SC 29208 USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Dept Med, Ctr Human Genet, Box 3445,595 LaSalle St, Durham, NC 27710 USA. EM mpv@chg.duhs.duke.edu RI Haines, Jonathan/C-3374-2012; Sutcliffe, James/C-1348-2012 OI Sutcliffe, James/0000-0001-5200-6007 CR Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Horvath S, 2004, GENET EPIDEMIOL, V26, P61, DOI 10.1002/gepi.10295 Palferman S, 2001, AM J HUM GENET, V69, P570 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 Rabionet R, 2004, NEUROSCI LETT, V372, P209, DOI 10.1016/j.neulet.2004.09.037 Ramoz N, 2004, AM J PSYCHIAT, V161, P662, DOI 10.1176/appi.ajp.161.4.662 NR 6 TC 1 Z9 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAY PY 2006 VL 163 IS 5 BP 929A EP 931 PG 3 WC Psychiatry SC Psychiatry GA 037GV UT WOS:000237136000032 ER PT J AU Murphy, DGM Daly, E Schmitz, N Toal, F Murphy, K Curran, S Erlandsson, K Eersels, J Kerwin, R Ell, P Travis, M AF Murphy, DGM Daly, E Schmitz, N Toal, F Murphy, K Curran, S Erlandsson, K Eersels, J Kerwin, R Ell, P Travis, M TI Cortical serotonin 5-HT(2A) receptor binding and social communication in adults with Asperger's syndrome: An in vivo SPECT study SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID PHOTON-EMISSION-TOMOGRAPHY; AUTISTIC DISORDER; BRAIN AB Objective: The cause of autistic spectrum disorder (i.e., autism and Asperger's syndrome) is unknown. The serotonergic (5-HT) system may be especially implicated. However, cortical 5-HT(2A) receptor density in adults with the disorder has not been examined, to the authors' knowledge. Method: The authors investigated cortical 5-HT(2A) receptor binding in eight adults with Asperger's syndrome and in 10 healthy comparison subjects with single photon emission computed tomography and the selective 5-HT(2A) receptor ligand 123I iodinated 4-amino-N-[1-[3-(4-fluorophenoxy)propyl]-4-methyl- 4-piperidinyl]-5-iodo-2-methoxybenzamide ((123)I-5-I-R91150). Results: People with Asperger's syndrome had a significant reduction in cortical 5-HT(2A) receptor binding in the total, anterior, and posterior cingulate; bilaterally in the frontal and superior temporal lobes; and in the left parietal lobe. Also, reduced receptor binding was significantly related to abnormal social communication. Conclusions: The authors' findings suggest that adults with Asperger's syndrome have abnormalities in cortical 5-HT(2A) receptor density and that this deficit may underlie some clinical symptoms. C1 Inst Psychiat, Dept Psychol Med, London SE5 8AF, England. Coll Surg, Dept Psychiat, Dublin, Ireland. UCL, Middlesex Hosp, London WC1E 6BT, England. Vrije Univ Amsterdam, Radionuclide Ctr, Amsterdam, Netherlands. RP Murphy, DGM (reprint author), Inst Psychiat, Dept Psychol Med, De Crespigny Pk,P50, London SE5 8AF, England. EM sphadgm@iop.kcl.ac.uk RI Schmitz, Nicole /F-9471-2011; daly, eileen/B-6716-2011; Murphy, Kieran/D-3577-2012 OI Schmitz, Nicole /0000-0003-4178-4756; CR AbiDargham A, 1997, EUR J PHARMACOL, V321, P285, DOI 10.1016/S0014-2999(96)00906-5 Busatto GF, 1997, EUR J NUCL MED, V24, P119, DOI 10.1007/BF02439542 COOK EH, 1993, LIFE SCI, V52, P2005, DOI 10.1016/0024-3205(93)90685-V Hariri AR, 2002, SCIENCE, V297, P400, DOI 10.1126/science.1071829 Jones HM, 2001, PSYCHOPHARMACOLOGY, V157, P60, DOI 10.1007/s002130100761 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 McAlonan GM, 2002, BRAIN, V125, P1594, DOI 10.1093/brain/awf150 MCBRIDE PA, 1989, ARCH GEN PSYCHIAT, V46, P213 McDougle CJ, 1996, ARCH GEN PSYCHIAT, V53, P1001 Moresco FM, 2002, NEUROIMAGE, V17, P1470, DOI 10.1006/nimg.2002.1239 Murphy DGM, 2002, ARCH GEN PSYCHIAT, V59, P885, DOI 10.1001/archpsyc.59.10.885 Stein DJ, 2002, LANCET, V360, P397, DOI 10.1016/S0140-6736(02)09620-4 Veenstra-VanderWeele J, 2002, AM J MED GENET, V114, P277, DOI 10.1002/ajmg.10192 Whitaker-Azmitia PM, 2001, BRAIN RES BULL, V56, P479, DOI 10.1016/S0361-9230(01)00615-3 NR 14 TC 82 Z9 83 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAY PY 2006 VL 163 IS 5 BP 934 EP 936 DI 10.1176/appi.ajp.163.5.934 PG 3 WC Psychiatry SC Psychiatry GA 037GV UT WOS:000237136000034 PM 16648340 ER PT J AU Drager, KDR Postal, VJ Carrolus, L Castellano, M Gagliano, C Glynn, J AF Drager, Kathryn D. R. Postal, Valerie J. Carrolus, Leanne Castellano, Megan Gagliano, Christine Glynn, Jennifer TI The effect of aided language modeling on symbol comprehension and production in 2 preschoolers with autism SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Article DE aided language modeling; intervention; autism; augmentative and alternative communication; symbols; comprehension; production ID MENTAL-RETARDATION; CHILDREN; DISABILITIES; ACQUISITION; MODERATE; YOUTH AB Purpose: The purpose of the present study was to examine the effectiveness of an instructional procedure called aided language modeling (ALM) on symbol comprehension and expression in 2 preschool children with autism who used few words functionally. ALM consists of engaging the child in interactive play activities and providing models of use of augmentative and alternative communication symbols during play. Method: A multiple-baseline design across sets of symbol vocabulary was used with 2 children who had autism. Four vocabulary items were taught in each of 3 legs of the design, for each child. Results: Both participants demonstrated increased symbol comprehension and elicited symbol production. In addition, both participants demonstrated that symbol comprehension and symbol production could be maintained. For both children, performance on symbol production lagged behind rate of responses on symbol comprehension. Conclusions: The current research presents preliminary evidence that a modeling intervention may be effective in increasing symbol comprehension and production, and may be an appropriate intervention strategy for some preschoolers with autism. Future research should continue to investigate this strategy and its effects on functional communication. C1 Penn State Univ, Dept Commun Sci & Disorders, University Pk, PA 16802 USA. Cent Susquehanna Intermediate Unit, Lewisburg, PA USA. RP Drager, KDR (reprint author), Penn State Univ, Dept Commun Sci & Disorders, 110 Moore Bldg, University Pk, PA 16802 USA. EM kdd5@psu.edu CR Alpert C. L., 1985, TEACHING FUNCTIONAL, P123 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bondy A. 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A., 1996, BREAKING SPEECH BARR Romski MA, 1996, AM J MENT RETARD, V100, P391 Rumbaugh DM, 1977, LANGUAGE LEARNING CH SCHLOSSER R, 1996, 4 INT SOC AUGM ALT C Schlosser RW, 1995, J APPL BEHAV ANAL, V28, P537, DOI 10.1901/jaba.1995.28-537 Schopler E., 1988, CHILDHOOD AUTISM RAT Schuler A. L., 1981, LANG SPEECH HEAR SER, V12, P246 SEVCIK RA, 1995, J SPEECH HEAR RES, V38, P902 Wing L., 1987, HDB AUTISM PERVASIVE, P3 Wood LA, 1998, AUGMENTATIVE ALTERNA, V14, P261, DOI 10.1080/07434619812331278436 NR 41 TC 23 Z9 25 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 1058-0360 J9 AM J SPEECH-LANG PAT JI Am. J. Speech-Lang. Pathol. PD MAY PY 2006 VL 15 IS 2 BP 112 EP 125 DI 10.1044/1058-0360(2006/012) PG 14 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 047GT UT WOS:000237868500003 PM 16782684 ER PT J AU Miller, CA AF Miller, Carol A. TI Developmental relationships between language and theory of mind SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Article DE cognition; normal language development; language disorders; autism spectrum disorders ID FALSE BELIEF TASK; JOINT ATTENTION; SOCIAL COGNITION; MENTAL STATE; INDIVIDUAL-DIFFERENCES; CHILDRENS KNOWLEDGE; SPEAKING CHILDREN; PEOPLES FEELINGS; AUTISM; PERFORMANCE AB Purpose: This tutorial is intended to inform readers about the development of theory of mind (understanding of mental states) and to discuss relationships between theory of mind and language development. Method: A narrative review of selected literature on language and theory of mind is presented. Theory of mind is defined, and commonly used measures of theory of mind are described. Developmental relationships between language and theory of mind in typical and atypical populations are discussed. Literature-based suggestions for clinical assessment and intervention are provided, using a hypothetical case study. Conclusions: The article serves as an introduction to current research about language and theory of mind, and emphasizes their interdependence in development. Implications of the relationships between theory of mind and language development for language assessment and intervention are discussed, and an argument is made that taking theory of mind into account will help clinicians enhance children's communication and language development. C1 Penn State Univ, Dept Commun Sci & Disorders, University Pk, PA 16802 USA. RP Miller, CA (reprint author), Penn State Univ, Dept Commun Sci & Disorders, 110 Moore Bldg, University Pk, PA 16802 USA. EM cam47@psu.edu CR Appleton M, 1996, SOC DEV, V5, P275, DOI 10.1111/j.1467-9507.1996.tb00086.x Astington J. W., 2005, WHY LANGUAGE MATTERS, P163 Astington J. W., 1993, CHILDS DISCOVERY MIN Astington J. 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J. Speech-Lang. Pathol. PD MAY PY 2006 VL 15 IS 2 BP 142 EP 154 DI 10.1044/1058-0360(2006/014) PG 13 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 047GT UT WOS:000237868500005 PM 16782686 ER PT J AU Abbeduto, L Murphy, MM Richmond, EK Amman, A Beth, P Weissman, MD Kim, JS Cawthon, SW Karadottir, S AF Abbeduto, L Murphy, MM Richmond, EK Amman, A Beth, P Weissman, MD Kim, JS Cawthon, SW Karadottir, S TI Collaboration in referential communication: Comparison of youth with down syndrome or fragile X syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID MENTAL-RETARDATION; YOUNG-CHILDREN; BEHAVIORAL-PHENOTYPE; RETARDED ADOLESCENTS; LANGUAGE-SKILLS; INDIVIDUALS; AUTISM; MIND; ADULTS; SENSORIMOTOR AB Referential communication was examined in youth with Down syndrome or fragile X syndrome in comparison to each other and to MA-matched typically developing children. 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PD MAY PY 2006 VL 111 IS 3 BP 170 EP 183 DI 10.1352/0895-8017(2006)111[170:CIRCCO]2.0.CO;2 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 046UI UT WOS:000237836200002 PM 16597184 ER PT J AU Lecavalier, L Aman, MG Scahill, L McDougle, CJ McCracken, JT Vitiello, B Tierney, E Arnold, LE Ghuman, JK Loftin, RL Cronin, P Koenig, K Posey, DJ Martin, A Hollway, J Lee, LS Kau, ASM AF Lecavalier, L Aman, MG Scahill, L McDougle, CJ McCracken, JT Vitiello, B Tierney, E Arnold, LE Ghuman, JK Loftin, RL Cronin, P Koenig, K Posey, DJ Martin, A Hollway, J Lee, LS Kau, ASM TI Validity of the autism diagnostic interview-revised SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID RATING-SCALE; BEHAVIOR CHECKLIST; CHILDHOOD AUTISM; ADI-R; CHILDREN; CLASSIFICATION; INDIVIDUALS; INSTRUMENTS; DISORDERS; SPECTRUM AB The factor structure, internal consistency, and convergent validity of the Autism Diagnostic Interview-Revised (ADI-R) algorithm items were examined in a sample of 226 youngsters with pervasive developmental disabilities. Exploratory factor analyses indicated a three-factor solution closely resembling the original algorithm and explaining 38% of the variance, with one significant discrepancy: Unlike the algorithm, all nonverbal communication items were associated with the Social factor. Internal consistencies of domain scores ranged from .54 to .84. Correlations between ADI-R domain and total scores and instruments assessing adaptive behavior, psychopathology, and autism were examined. They indicated some similarities between constructs, but also that the ADI-R measures autism in a unique fashion. C1 Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. Indiana Univ, Riley Hosp Children, Bloomington, IN 47405 USA. Univ Calif Los Angeles, Inst Neuropsychiat, Los Angeles, CA 90024 USA. NIMH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Kennedy Krieger Inst, Baltimore, MD 21218 USA. 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J. Ment. Retard. PD MAY PY 2006 VL 111 IS 3 BP 199 EP 215 DI 10.1352/0895-8017(2006)111[199:VOTADI]2.0.CO;2 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 046UI UT WOS:000237836200006 PM 16597187 ER PT J AU Ashley-Koch, AE Mei, H Jaworski, J Ma, DQ Ritchie, MD Menold, MM Delong, GR Abramson, RK Wright, HH Hussman, JP Cuccaro, ML Gilbert, JR Martin, ER Pericak-Vance, MA AF Ashley-Koch, AE Mei, H Jaworski, J Ma, DQ Ritchie, MD Menold, MM Delong, GR Abramson, RK Wright, HH Hussman, JP Cuccaro, ML Gilbert, JR Martin, ER Pericak-Vance, MA TI An analysis paradigm for investigating multi-locus effects in complex disease: Examination of three GABA(A) receptor subunit genes on 15q11-q13 as risk factors for autistic disorder. SO ANNALS OF HUMAN GENETICS LA English DT Article ID LINKAGE DISEQUILIBRIUM; CHROMOSOME 15Q11-Q13; INFANTILE-AUTISM; ASSOCIATION; FAMILIES; EPILEPSY; TESTS; TWIN; PEDIGREES; GENETICS AB Gene-gene interactions are likely involved in many complex genetic disorders and new statistical approaches for detecting such interactions are needed. We propose a multi-analytic paradigm, relying on convergence of evidence across multiple analysis tools. Our paradigm tests for main and interactive effects, through allele, genotype and haplotype association. We applied our paradigm to genotype data from three GABA(A) receptor subunit genes (GABRB3, GABRA5, and GABRG3) on chromosome 15 in 470 Caucasian autism families. Previously implicated in autism, we hypothesized these genes interact to contribute to risk. We detected no evidence of main effects by allelic (PDT, FBAT) or genotypic (genotype-PDT) association at individual markers. However, three two-marker haplotypes in GABRG3 were significant (HBAT). We detected no significant multi-locus associations using genotype-PDT analysis or the EMDR data reduction program. However, consistent with the haplotype findings, the best single locus EMDR model selected a GABRG3 marker. Further, the best pairwise genotype-PDT result involved GABRB3 and GABRG3, and all multi-locus EMDR models also selected GABRB3 and GABRG3 markers. GABA receptor subunit genes do not significantly interact to contribute to autism risk in our overall data set. However, the consistency of results across analyses suggests that we have defined a useful framework for evaluating gene-gene interactions. C1 Duke Univ, Med Ctr, Ctr Human Genet, Dept Med, Durham, NC 27710 USA. Vanderbilt Univ, Vanderbilt Ctr Human Genet Res, Nashville, TN USA. Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. WS Hall Psychiat Inst, Columbia, SC USA. John P Hussman Fdn, Ellicott City, MD USA. RP Ashley-Koch, AE (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Dept Med, Box 3400,2007 Snyderman Genom Sci Bldg,595 LaSall, Durham, NC 27710 USA. 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D., 1998, PHENOTYPIC EVOLUTION Schroer RJ, 1998, AM J MED GENET, V76, P327, DOI 10.1002/(SICI)1096-8628(19980401)76:4<327::AID-AJMG8>3.0.CO;2-M Shao YJ, 2003, AM J HUM GENET, V72, P539, DOI 10.1086/367846 Shao YJ, 2002, AM J MED GENET, V114, P99, DOI 10.1002/ajmg.10153 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Templeton AR, 2000, EPISTASIS EVOLUTIONA, P41 THOMSON G, 1995, AM J HUM GENET, V57, P487 Tuchman R, 2002, LANCET NEUROL, V1, P352, DOI 10.1016/S1474-4422(02)00160-6 Vance Jeffery M., 1998, P201 Wallace RH, 2001, NAT GENET, V28, P49, DOI 10.1038/ng0501-49 Wolpert CM, 2000, AM J MED GENET, V96, P365, DOI 10.1002/1096-8628(20000612)96:3<365::AID-AJMG25>3.0.CO;2-X WRIGHT SEWALL, 1932, PROC SIXTH INTERNAT CONGR GENETICS ITHACA NEW YORK, V1, P356 ZAYKIN D, 1995, GENETICA, V96, P169, DOI 10.1007/BF01441162 NR 46 TC 34 Z9 35 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0003-4800 J9 ANN HUM GENET JI Ann. Hum. Genet. PD MAY PY 2006 VL 70 BP 281 EP 292 DI 10.1111/j.1469-1809.2006.00253.x PN 3 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA 031XF UT WOS:000236737800001 PM 16674551 ER PT J AU Chavez, B Chavez-Brown, M Rey, JA AF Chavez, B Chavez-Brown, M Rey, JA TI Role of risperidone in children with autism spectrum disorder SO ANNALS OF PHARMACOTHERAPY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; LONG-TERM RISPERIDONE; OPEN-LABEL; CASE SERIES; ADOLESCENTS; OLANZAPINE; ADULTS; DISCONTINUATION; QUETIAPINE; TRIAL AB OBJECTIVE: To review the clinical trials investigating the efficacy and safety of risperidone in the treatment of children with autism spectrum disorder (ASD). DATA SOURCES: Searches of MEDLINE/PubMed (1992-February 2006) were conducted, as well as an extensive manual review of journals, using the key words autism and risperidone. STUDY SELECTION AND DATA E)EXTRACTION: Only double-blind, placebo-controlled trials were included for review. DATA SYNTHESIS: ASD is the most common of the pervasive developmental disorders. The main characteristics (core symptoms) of autism are impairment in social skills, problems communicating, and stereotypical movements. Behavioral manifestations or maladaptive behaviors include aggression, irritability, hyperactivity, inattention, impulsivity, tantrums, and self-injurious behavior. CONCLUSIONS: Based on the data examined, risperidone appears efficacious and safe for treating certain behavioral aspects of autism including irritability, aggression, hyperactivity, and stereotypy. It does not appear to be as effective for the treatment of the core symptoms of autism. C1 Rutgers State Univ, Ernest Mario Sch Pharm, Piscataway, NJ 08854 USA. Wagner Coll, Dept Educ, Staten Isl, NY 10301 USA. Nova SE Univ, Coll Pharm, Ft Lauderdale, FL 33314 USA. RP Chavez-Brown, M (reprint author), Rutgers State Univ, Ernest Mario Sch Pharm, 160 Frelinghuysen Way, Piscataway, NJ 08854 USA. 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Pharmacother. PD MAY PY 2006 VL 40 IS 5 BP 909 EP 916 DI 10.1345/aph.1G389 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 043KW UT WOS:000237600900013 PM 16684811 ER PT J AU Rivara, FP AF Rivara, FP TI Autism and autism spectrum disorders SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Editorial Material C1 Univ Washington, Dept Pediat, Inst Child Hlth, Seattle, WA 98115 USA. RP Rivara, FP (reprint author), Univ Washington, Dept Pediat, Inst Child Hlth, 6200 NE 74th St,Suite 210, Seattle, WA 98115 USA. EM archpediatrics@jama-archives.org NR 0 TC 0 Z9 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD MAY PY 2006 VL 160 IS 5 BP 548 EP 548 DI 10.1001/archpedi.160.5.548-a PG 1 WC Pediatrics SC Pediatrics GA 038JK UT WOS:000237215600016 ER PT J AU Eaves, LC Wingert, H Ho, HH AF Eaves, LC Wingert, H Ho, HH TI Screening for autism - Agreement with diagnosis SO AUTISM LA English DT Article DE autism spectrum disorders; modified checklist for autism in toddlers; screening tools; social communication questionnaire ID PERVASIVE DEVELOPMENTAL DISORDERS; INSTRUMENT; INTERVIEW; CHECKLIST; TODDLERS AB Screening measures to identify very young children at risk for autism spectrum disorders include the Modified Checklist for Autism in Toddlers (M-CHAT) and the Social Communication Questionnaire (SCQ). To examine the validity of these written questionnaires, parents completed them prior to their child's diagnostic assessment at a tertiary autism clinic. The M-CHAT was given to 84 parents of 2- to 3-year-olds and the SCQ to 94 parents of 4- to 6-year-olds. On both measures sensitivity was higher than specificity with positive predictive values 0.63-0.68. False negatives, or children with autism who were missed by screening, were somewhat higher functioning than true positives. Results were better for parents who spoke English as a second language, contrary to expectations. At this stage of development these tools would be recommended as part of more comprehensive surveillance programmes to identify children in need of further assessment but not to 'screen out' the possibility of autism. C1 Sunny Hill Vet Ctr, Vancouver, BC, Canada. RP Eaves, LC (reprint author), Sunny Hill Vet Ctr, Vancouver, BC, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Baird G, 2001, ARCH DIS CHILD, V84, P468, DOI 10.1136/adc.84.6.468 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 CORSELLO C, 2006, SOC RES CHILD DEV BI Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 HANSON E, 2002, INT M AUT RES NOV LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LECOUTEUR A, 2003, AUTISM DIAGNOSTIC IN LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Robins DL, 2001, J AUTISM DEV DISORD, V31, P131, DOI 10.1023/A:1010738829569 Rutter M., 2003, SOCIAL COMMUNICATION SAESMUNDSEN E, 2003, J AUTISM DEV DISORD, V33, P319 Scambler D, 2001, J AM ACAD CHILD PSY, V40, P1457, DOI 10.1097/00004583-200112000-00017 Schopler E., 1988, CHILDHOOD AUTISM RAT NR 16 TC 42 Z9 42 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAY PY 2006 VL 10 IS 3 BP 229 EP 242 DI 10.1177/1362361306063288 PG 14 WC Psychology, Developmental SC Psychology GA 051VO UT WOS:000238190000002 PM 16682396 ER PT J AU Turner, LM Stone, WL Pozdol, SL Coonard, EE AF Turner, LM Stone, WL Pozdol, SL Coonard, EE TI Follow-up of children with autism spectrum disorders from age 2 to age 9 SO AUTISM LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; YOUNG-CHILDREN; JOINT ATTENTION; STABILITY; COMMUNICATION; PREDICTORS; CONTINUITY; PARAMETERS; LEVEL AB The purpose of the present study was to examine the developmental outcomes of children 7 years after their initial diagnosis. Children diagnosed with autism or PDD-NOS at age 2 received follow-up evaluations at age 9. Diagnostic stability was high, with 88 percent of the sample obtaining autism spectrum diagnoses at age 9. Cognitive scores improved considerably for a large segment of the sample, with over 50 percent obtaining scores in the average range at follow-up. Language outcomes were also positive at follow-up; 88 percent of the sample demonstrated at least some functional language, and 32 percent were able to engage in conversational exchanges. Early characteristics that predicted outcome status were: age of diagnosis, age 2 cognitive and language scores, and total hours of speech-language therapy between ages 2 and 3. These findings highlight the potential long-term benefits of both early identification and early intervention, and provide additional evidence for the importance of promoting public awareness of the early signs of autism. C1 Vanderbilt Univ, Nashville, TN 37240 USA. RP Turner, LM (reprint author), Vanderbilt Univ, 221 Kirkland Hall, Nashville, TN 37240 USA. 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SO AUTISM LA English DT Article DE Asperger syndrome; children's communication; checklist cluster; analysis high-functioning autism; pervasive developmental disorder not otherwise specified ID PERVASIVE DEVELOPMENTAL DISORDER; ASPERGER-SYNDROME; LANGUAGE DISORDERS; CLUSTER-ANALYSIS; PDD-NOS; CLASSIFICATION; INDIVIDUALS; IMPAIRMENT; DIAGNOSIS; SPEECH AB The study explored whether children with high-functioning autism (HFA), Asperger syndrome (AS), and pervasive developmental disorder not otherwise specified (PDD-NOS) can be differentiated on the Children's Communication Checklist (CCC). The study also investigated whether empirically derived autistic subgroups can be identified with a cluster analytic method based on the Autism Diagnostic Interview-Revised. Fifty-seven children with HFA, 47 with AS, 31 with PDD-NOS, and a normal control group of 47 children between 6 and 13 years participated. Children with HFA, AS, and PDD-NOS showed pragmatic communication deficits in comparison to the controls. Little difference was found between the three subtypes with respect to their CCC profile. A three-cluster solution explained the data best. The HFA cluster showed most autism characteristics, followed by the combined HFA + AS cluster, and then the PDD-NOS cluster. The findings support the autism spectrum concept based on severity of symptom impairment rather than distinct categories. C1 Univ Ghent, B-9000 Ghent, Belgium. Vrije Univ Amsterdam, NL-1081 HV Amsterdam, Netherlands. RP Verte, S (reprint author), Univ Ghent, B-9000 Ghent, Belgium. 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Yoder, Paul J. Stone, Wendy L. TI Labels increase attention to novel objects in children with autism and comprehension-matched children with typical development SO AUTISM LA English DT Article DE attention following autism; language development; word learning ID JOINT ATTENTION; NONVERBAL-COMMUNICATION; EARLY LANGUAGE; DOWN-SYNDROME; INFANTS; COMPETENCE; COGNITION; AGE AB This study used an intact group comparison to examine attention following in 34 children aged 2 years diagnosed with autism spectrum disorder (ASD) matched pairwise for vocabulary comprehension with a group of typically developing toddlers. For both groups of children, the presence of verbal labels during a referential task increased attention to a novel object over and above the attention-facilitating effect of child-directed talking without labeling. The typically developing children displayed more attention following than comprehension-matched children with ASD across experimental conditions and there was no significant difference between the groups in the facilitative effect of hearing verbal labels. Implications for word-learning theory, intervention strategies and future research are considered. C1 Univ Wisconsin, Madison, WI 53706 USA. Vanderbilt Univ, Vanderbilt Childrens Hosp, Nashville, TN 37240 USA. RP McDuffie, AS (reprint author), Univ Wisconsin, Madison, WI 53706 USA. 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K., 1989, ANAL QUANTITATIVE BE TAPP J, 1995, BEHAV RES METH INSTR, V27, P25, DOI 10.3758/BF03203616 TAPP J, 2003, PROCODER DV COMPUTER Tincoff R, 1999, PSYCHOL SCI, V10, P172, DOI 10.1111/1467-9280.00127 Tomasello M, 2003, MIND LANG, V18, P121, DOI 10.1111/1468-0017.00217 Tomasello M., 2001, LANG ACQUIS, P133 Woodward J.Z., 1990, M INT C INF STUD MON Yoder PJ, 1999, J EARLY INTERVENTION, V22, P126 NR 40 TC 9 Z9 9 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 EI 1461-7005 J9 AUTISM JI Autism PD MAY PY 2006 VL 10 IS 3 BP 288 EP 301 DI 10.1177/1362361306063287 PG 14 WC Psychology, Developmental SC Psychology GA 051VO UT WOS:000238190000005 PM 16682399 ER PT J AU Feroz-Nainar, C Selvaraj, P Roy, M AF Feroz-Nainar, C Selvaraj, P Roy, M TI Risperidone induced oedema in a child with learning disability and autism SO AUTISM LA English DT Article EM doctorferoz@yahoo.co.uk CR Baldassano CF, 1996, J CLIN PSYCHIAT, V57, P422 *BRIT MED ASS, 2002, BRIT NAT FORM Katz IR, 1999, J CLIN PSYCHIAT, V60, P107 Ravasia S, 2001, CAN J PSYCHIAT, V46, P453 Sanders RD, 1998, J CLIN PSYCHIAT, V59, P689, DOI 10.4088/JCP.v59n1208e STAHL MS, 1999, PSYCHOPHARMACOLOGY A Tamam L, 2002, CLIN DRUG INVEST, V22, P411, DOI 10.2165/00044011-200222060-00011 Terao T, 1998, J CLIN PSYCHIAT, V59, P82, DOI 10.4088/JCP.v59n0207c NR 8 TC 6 Z9 6 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAY PY 2006 VL 10 IS 3 BP 308 EP 310 DI 10.1177/1362361306063302 PG 3 WC Psychology, Developmental SC Psychology GA 051VO UT WOS:000238190000007 PM 16682401 ER PT J AU Matthews, V AF Matthews, V TI Being responsive: You and your child with autism SO AUTISM LA English DT Book Review C1 Islington PCT, London, England. RP Matthews, V (reprint author), Islington PCT, London, England. CR KEEN D, 2005, BEING YOU YOUR RESPO NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAY PY 2006 VL 10 IS 3 BP 311 EP 312 DI 10.1177/1362361306063305 PG 2 WC Psychology, Developmental SC Psychology GA 051VO UT WOS:000238190000008 ER PT J AU Arndt, TL Chadman, KK Watson, DJ Tsang, V Rodier, PM Stanton, ME AF Arndt, TL Chadman, KK Watson, DJ Tsang, V Rodier, PM Stanton, ME TI Long delay eyeblink conditioning in autism SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY LA English DT Meeting Abstract C1 Univ Rochester, Sch Med & Dent, Rochester, NY 14627 USA. Univ Delaware, Newark, DE USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1542-0752 J9 BIRTH DEFECTS RES A JI Birth Defects Res. Part A-Clin. Mol. Teratol. PD MAY PY 2006 VL 76 IS 5 MA 18 BP 323 EP 323 PG 1 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA 048GS UT WOS:000237936200019 ER PT J AU Herbert, MR AF Herbert, MR TI Autism: Parsing heterogeneity of causes and features SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1542-0752 J9 BIRTH DEFECTS RES A JI Birth Defects Res. Part A-Clin. Mol. Teratol. PD MAY PY 2006 VL 76 IS 5 MA S1 BP 342 EP 342 PG 1 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA 048GS UT WOS:000237936200052 ER PT J AU Briesacher, BA Orwig, D Seton, M Omar, M Kahler, KH AF Briesacher, Becky A. Orwig, Denise Seton, Margaret Omar, Mohamed Kahler, Kristijan H. TI Medical care costs of Paget's disease of bone in a privately insured population SO BONE LA English DT Article DE reelin; association; LD; PDT; autism ID UNITED-STATES; MANAGEMENT; MANIFESTATIONS; COMORBIDITIES; COMPLICATIONS; FRACTURES; FEATURES; THERAPY; ENGLAND; HEALTH AB Introduction: Medical care costs are difficult to calculate in diseases such as Paget's disease because they have low detection rates and a wide range of clinical manifestations that commonly occur in aging patient populations. Materials and methods: Using 2001-2002 MarketScan Research databases, this study linked medical claims, prescription records, and encounter data on 2.8 million active and retired employees to create a longitudinal panel with 24 months of observation. Patients with Paget's disease were identified by ICD-9 code 731.0. Matched controls (MC) were identified through an exact match procedure using gender, age, and predicted Medicare costs estimated with a risk adjuster. Diagnostic and expenditure records were extracted for the sample and prevalence rates calculated for 20 conditions with well-documented associations to Paget's disease. Comorbidities and health care costs of Paget's disease patients were compared to those of the MCs, and the differences tested using Chi-square and t tests. Results: Our study identified 244 matched pairs. The average age was 72.7 years; 50.8% were female. Significantly higher comorbidities (P < 0.05) were detected in Paget's disease patients relative to MCs for: pathological fractures (4.9% vs. 0.4%), heart murmurs (3.3% vs. 0.4%), low back pain (19.7% vs. 8.6%), spinal stenosis (16.4% vs. 9.8%), and hearing loss (13.5% vs. 5.7%), respectively. Biannual per patient outpatient costs were significantly higher in Paget's disease patients (Paget's disease $9301 vs. MC $6339, P < 0.05), especially for services associated with physician visits and diagnostic tests. Prescription costs for antiresportive agents and analgesics were also higher (Paget's disease $1115 vs. MC $507, P < 0.05). Inpatient costs (Paget's disease $16,144 vs. MC $21.480) were comparable. Conclusion: This study is the first to describe the excessive costs of Paget's disease, based on known patterns of disease expression, evaluation, and treatment. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ Massachusetts, Sch Med, Div Geriatr Med, Biotech 4, Worcester, MA 01605 USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. Massachusetts Gen Hosp, Boston, MA 02129 USA. Novartis Pharmaceut Corp, E Hanover, NJ 07936 USA. RP Briesacher, BA (reprint author), Univ Massachusetts, Sch Med, Div Geriatr Med, Biotech 4, Suite 315,377 Plantat St, Worcester, MA 01605 USA. EM Becky.Briesacher@umassmed.edu; DORWIG@epi.umaryland.edu; margaret_seton@hms.harvard.edu; mohamed.omar@novartis.com; Kristijan.Kahler@novartis.com CR Ahmed F, 2005, J CLIN EPIDEMIOL, V58, P624, DOI 10.1016/j.jclinepi.2004.11.020 Altman RD, 2000, J BONE MINER RES, V15, P461, DOI 10.1359/jbmr.2000.15.3.461 ALTMAN RD, 1980, ARTHRITIS RHEUM, V23, P1121, DOI 10.1002/art.1780231008 Ankrom MA, 1998, J AM GERIATR SOC, V46, P1025 Ash AS, 2000, HEALTH CARE FINANC R, V21, P7 Borzecki AM, 2004, AM J MED QUAL, V19, P201, DOI 10.1177/106286060401900504 Delmas PD, 1997, NEW ENGL J MED, V336, P558 DOVE J, 1980, J BONE JOINT SURG BR, V62, P12 Drake WM, 2001, CLIN THER, V23, P620, DOI 10.1016/S0149-2918(01)80065-5 Etzioni R, 2002, MED CARE, V40, P63 FRANCK WA, 1974, AM J MED, V56, P592, DOI 10.1016/0002-9343(74)90629-9 Gabriel SE, 2002, OSTEOPOROSIS INT, V13, P323, DOI 10.1007/s001980200033 Gold DT, 1999, J BONE MINER RES, V14, P99 Gold DT, 1996, J BONE MINER RES, V11, P1897 GRUNDY M, 1970, Journal of Bone and Joint Surgery British Volume, V52, P252 HAMDY RC, 1993, SOUTHERN MED J, V86, P1097, DOI 10.1097/00007611-199310000-00003 Hu XH, 1999, ARCH INTERN MED, V159, P813, DOI 10.1001/archinte.159.8.813 Keen RW, 2003, HOSP MED, V64, P230 Lafuma A, 1997, PHARMACOECONOMICS, V12, P460, DOI 10.2165/00019053-199712040-00004 Langston AL, 2004, RHEUMATOLOGY, V43, P955, DOI 10.1093/rheumatology/keh243 Mark TL, 2003, HEALTH AFFAIR, V22, P165, DOI 10.1377/hlthaff.22.1.165 Melton LJ, 2000, J BONE MINER RES, V15, P2123, DOI 10.1359/jbmr.2000.15.11.2123 Menzin J, 1999, AM J GERIAT PSYCHIAT, V7, P300 MIRRA JM, 1995, SKELETAL RADIOL, V24, P173 Newton KM, 1999, J CLIN EPIDEMIOL, V52, P199, DOI 10.1016/S0895-4356(98)00161-9 Ooi CG, 1997, POSTGRAD MED J, V73, P69 Saifuddin A, 2003, CLIN RADIOL, V58, P102, DOI 10.1053/crad.2003.1152 Schneider D, 2002, AM FAM PHYSICIAN, V65, P2069 Selby PL, 2002, BONE, V31, P366, DOI 10.1016/S8756-3282(02)00817-7 Seton M, 1997, Curr Ther Endocrinol Metab, V6, P568 Seton M, 2003, J BONE MINER RES, V18, P1519, DOI 10.1359/jbmr.2003.18.8.1519 Tiegs RD, 1997, CLIN THER, V19, P1309, DOI 10.1016/S0149-2918(97)80007-0 Tiegs RD, 2000, BONE, V27, P423, DOI 10.1016/S8756-3282(00)00333-1 Van Staa TP, 2002, J BONE MINER RES, V17, P465, DOI 10.1359/jbmr.2002.17.3.465 NR 34 TC 8 Z9 8 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 8756-3282 J9 BONE JI Bone PD MAY PY 2006 VL 38 IS 5 BP 731 EP 737 DI 10.1016/j.bone.2005.10.015 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 043PU UT WOS:000237614400016 PM 16364708 ER PT J AU Campbell, LE Daly, E Toal, F Stevens, A Azuma, R Catani, M Ng, V van Amelsvoort, T Chitnis, X Cutter, W Murphy, DGM Murphy, KC AF Campbell, LE Daly, E Toal, F Stevens, A Azuma, R Catani, M Ng, V van Amelsvoort, T Chitnis, X Cutter, W Murphy, DGM Murphy, KC TI Brain and behaviour in children with 22q11.2 deletion syndrome: a volumetric and voxel-based morphometry MRI study SO BRAIN LA English DT Article DE velo-cardio-facial syndrome ( VCFS); 22q11.2 deletion syndrome ( 22qDS); voxel; based morphometry; behaviour; children ID CARDIO-FACIAL SYNDROME; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; VELOCARDIOFACIAL-SYNDROME; CHROMOSOME 22Q11; NEUROPSYCHOLOGICAL PROFILE; SCHIZOPHRENIC-PATIENTS; SPECTRUM DISORDERS; MAJOR DEPRESSION; SYNDROME VCFS; ADULTS AB In people with velo-cardio-facial syndrome [or 22q11.2 deletion syndrome (22qDS)], a single interstitial deletion of chromosome 22q11.2 causes a wide spectrum of cognitive deficits ranging from global learning difficulties to specific cognitive deficits. People with 22qDS are also at high risk of developing attention-deficit/hyperactivity disorder and autism spectrum disorders in childhood, and schizophrenia in adolescence or adult life. However, the neurobiology of 22qDS, and the relationship between abnormalities in brain anatomy and behaviour, is poorly understood. Thus, we studied the neuroanatomy of 22qDS children using fully automated voxel-based morphometry (VBM) and manually traced single region-of-interest (ROI) analysis. Also, we investigated whether those brain regions that differed significantly between groups were related to behavioural differences within children with 22qDS. We compared the brain morphometry of 39 children and adolescents with 22qDS (mean age: 11 years, SD +/- 3, IQ = 67, SD +/- 10) and 26 sibling controls (mean age: 11 years, SD +/- 3, IQ = 102, SD +/- 12). Using VBM, we found, after correction for IQ, that individuals with 22qDS compared with controls had a significant reduction in cerebellar grey matter, and white matter reductions in the frontal lobe, cerebellum and internal capsule. Using single ROI analysis, we found that people with 22qDS had a significant (P < 0.05) reduction in bulk volume bilaterally in the occipital-parietal lobes, but a larger right caudate nucleus and lateral ventricles. Further, within people with 22qDS, there was a significant positive correlation between severity of (i) schizotypy score and grey matter volume of the temporo-occipital regions and the corpus striatum; (ii) emotional problems and grey matter volume of frontostriatal regions; and (iii) social behavioural difficulties and grey matter in frontostriatal regions. Thus, subjects with 22qDS have widespread changes in brain anatomy, particularly affecting white matter, basal ganglia and cerebellum. Also, within 22qDS, regionally specific differences in brain development may partially underpin behavioural differences. We suggest that there is preliminary evidence for specific vulnerability of the frontostriatal and cerebellar-cortical networks in 22qDS. C1 Royal Coll Surgeons Ireland, Dept Psychiat, Dublin 2, Ireland. Univ London Kings Coll, Inst Psychiat, London WC2R 2LS, England. Univ Amsterdam, Acad Med Ctr, Dept Psychiat, NL-1105 AZ Amsterdam, Netherlands. RP Campbell, LE (reprint author), Univ Newcastle, Jame Fletcher Hosp, Ctr Mental Hlth Studies, Newcastle, NSW 2300, Australia. 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Z9 101 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD MAY PY 2006 VL 129 BP 1218 EP 1228 DI 10.1093/brain/awl066 PN 5 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 035JV UT WOS:000236998000016 PM 16569671 ER PT J AU Koishi, S Yamamoto, K Matsumoto, H Koishi, S Enseki, Y Oya, A Asakura, A Aoki, Y Atsumi, M Iga, T Inomata, J Inoko, H Sasaki, T Nanba, E Kato, N Ishii, T Yamazaki, K AF Koishi, S Yamamoto, K Matsumoto, H Koishi, S Enseki, Y Oya, A Asakura, A Aoki, Y Atsumi, M Iga, T Inomata, J Inoko, H Sasaki, T Nanba, E Kato, N Ishii, T Yamazaki, K TI Serotonin transporter gene promoter polymorphism and autism: A family-based genetic association study in Japanese population SO BRAIN & DEVELOPMENT LA English DT Article DE autism; serotonin transporter (5-HTT); serotonin transporter gene promoter polymorphism; transmission/disequilibrium test; ethnic differences ID DISORDER; REGION; VARIANTS; LINKAGE; DISEQUILIBRIUM; 5-HTT AB Autism is now widely accepted as a biological disorder which, by and large, starts before birth. It has been shown that serotonin (5-HT) is associated with several psychological processes and hyperserotoninemia is observed in some autistic patients. The results of previous reports about family-based association studies between the serotonin transporter (5-HTT) gene promoter polymorphism and autism are controversial. In this study, an analysis using the transmission/disequilibrium test (TDT) between the 5-HTT gene promoter polymorphism and autism in 104 trios, all ethnically Japanese, showed no significant linkage disequilibrium (P = 0.17). Recently, it has been reported that some haplotypes at the serotonin transporter locus may be associated with the pathogenesis of autism. Therefore, further investigations by haplotype analyses are necessary to confirm the implications of genetic variants of the serotonin transporter in the etiology of autism. (c) 2005 Elsevier B.V. All rights reserved. C1 Tokai Univ, Sch Med, Course Specialized Clin Sci, Dept Psychiat, Isehara, Kanagawa 2591193, Japan. Tokai Univ, Sch Med, Dept Mol Life Sci, Isehara, Kanagawa 25911, Japan. Sodegaura Nobiro Gakuen, Chiba, Japan. Res Ctr Child Life, Tokyo, Japan. Univ Tokyo, Grad Sch Med, Dept Psychiat, Tokyo, Japan. Tottori Univ, Ctr Gene Res, Yonago, Tottori, Japan. RP Yamamoto, K (reprint author), Tokai Univ, Sch Med, Course Specialized Clin Sci, Dept Psychiat, Isehara, Kanagawa 2591193, Japan. 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PD MAY PY 2006 VL 28 IS 4 BP 257 EP 260 DI 10.1016/j.braindev.2005.09.003 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 031GO UT WOS:000236692800008 PM 16481140 ER PT J AU King, GA Zwaigenbaum, L King, S Baxter, D Rosenbaum, P Bates, A AF King, GA Zwaigenbaum, L King, S Baxter, D Rosenbaum, P Bates, A TI A qualitative investigation of changes in the belief systems of families of children with autism or Down syndrome SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE autism; Down syndrome; family; priorities; qualitative; world views ID PARENTING STRESS; DISABILITIES; RESILIENCE; PERSPECTIVES; ADAPTATION; CHALLENGE; DISORDERS; COHERENCE; OUTCOMES; SENSE AB There have been few reports of the world views, values and priorities of families of children with autism or Down syndrome, despite the fact that family belief systems are considered to be among the most important factors affecting the adaptation and resilience of families. Transcripts from three focus groups involving 19 key informants (15 parents of children with autism or Down syndrome, and 4 service providers) were analysed using qualitative methods. The themes indicated that raising a child with a disability can be a life-changing experience that spurs families to examine their belief systems. Parents can come to gain a sense of coherence and control through changes in their world views, values and priorities that involve different ways of thinking about their child, their parenting role, and the role of the family. Although parents may grapple with lost dreams, over time positive adaptations can occur in the form of changed world views concerning life and disability, and an appreciation of the positive contributions made by children to family members and society as a whole. Parents' experiences indicate the importance of hope and of seeing possibilities that lie ahead. 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PD MAY PY 2006 VL 32 IS 3 BP 353 EP 369 DI 10.1111/j.1365-2214.2006.00571.x PG 17 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 027DE UT WOS:000236393100010 PM 16634980 ER PT J AU Renty, J Roeyers, H AF Renty, J Roeyers, H TI Satisfaction with formal support and education for children with autism spectrum disorder: the voices of the parents SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Article DE autism spectrum disorders; diagnosis; education; parental satisfaction ID PRESCHOOL-CHILDREN; YOUNG-CHILDREN; SOCIAL SUPPORT; FOLLOW-UP; DISABILITIES; FAMILIES; DIAGNOSIS; SERVICE; MOTHERS; COMMUNICATION AB The aim of the present study was to identify and describe factors associated with variations in the level of parental satisfaction with formal support and education for children with autism spectrum disorder (ASD) in Flanders. Participants were recruited by a mailing from a diagnostic centre for pre-schoolers and by advertisements dispersed in the Flemish parent organization for ASD and in services and special schools. The sample consisted of 244 parents of children with ASD (age range: 2.69-17.81 years, male/female sex ratio 4 : 1). The data were collected using a questionnaire on experiences with education and support, which was compiled for the purpose of this study. The data resulting from the questionnaire were supplemented with information obtained from semi-structured in-depth interviews with a stratified sample of 15 parents. The study revealed that parents experienced difficulties with the diagnostic process, with support and education provided by mainstream settings and with the accessibility of autism-specific service provisions. Conversely, parents reported to be satisfied with the quality of autism-specific support and education. 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PD MAY PY 2006 VL 32 IS 3 BP 371 EP 385 DI 10.1111/j.1365-2214.2006.00584.x PG 15 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 027DE UT WOS:000236393100011 PM 16634981 ER PT J AU Tan, QR Wang, W Wang, HH Zhang, RG Guo, L Zhang, YH AF Tan, QR Wang, W Wang, HH Zhang, RG Guo, L Zhang, YH TI Treatment of catatonic stupor with combination of modified electroconvulsive treatment and olanzapine: A case report SO CLINICAL NEUROPHARMACOLOGY LA English DT Review DE modified electroconvulsive treatment (MECT); olanzapine; catatonic stupor ID SCHIZOPHRENIA; LORAZEPAM; THERAPY AB This case report is about the combined use of modified electroconvulsive treatment and an atypical antipsychotic drug, olanzapine, in the treatment of a 20-year-old man with chronic and refractory catatonic stupor. This patient, with a preexisting diagnosis of autism, posturing, nonverbal communication, and contracture of lower extremities, displaying mutism, akinesia, and an extreme level of rigidity, waxy flexibility, and posturing, was diagnosed as with catatonic stupor. After hospitalization, the disease had progressed despite the treatment with an atypical antipsychotic drug, olanzapine. Modified electroconvulsive treatment together with olanzapine caused a dramatic clinical improvement. Follow-up outpatient treatment with olanzapine improved his social functions. C1 Fourth Mil Med Univ, Xijing Hosp, Psychosomat Dept, Xian 710032, Peoples R China. Fourth Mil Med Univ, Dept Anat, Xian 710032, Peoples R China. Fourth Mil Med Univ, KK Leung Brain Res Ctr, Xian 710032, Peoples R China. RP Tan, QR (reprint author), Fourth Mil Med Univ, Xijing Hosp, Psychosomat Dept, 17 W Changle Rd, Xian 710032, Peoples R China. 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PD MAY-JUN PY 2006 VL 29 IS 3 BP 154 EP 156 DI 10.1097/01.WNF.0000220816.86478.84 PG 3 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA 050KG UT WOS:000238085700009 PM 16772815 ER PT J AU Margutti, P Delunardo, F Ortona, E AF Margutti, P Delunardo, F Ortona, E TI Autoantibodies associated with psychiatric disorders SO CURRENT NEUROVASCULAR RESEARCH LA English DT Review DE endothelium; central nervous system; blood-brain barrier; autoantigens; autoirnmunity; drug abusers; schizophrenia; autism; post-streptococcal diseases; celiac disease; chronic fatigue syndrome ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; CHRONIC-FATIGUE-SYNDROME; CENTRAL-NERVOUS-SYSTEM; POSTSTREPTOCOCCAL AUTOIMMUNE DISORDERS; OBSESSIVE-COMPULSIVE DISORDER; ENDOTHELIAL-CELL AUTOANTIGENS; MYELIN BASIC-PROTEIN; RIBOSOMAL P-PROTEIN; SCHIZOPHRENIC-PATIENTS; CELIAC-DISEASE AB Growing evidence suggests that autoantibodies to neuronal or endothelial targets in psychiatric disorders exist and may be pathogenic. 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Neurovasc. Res. PD MAY PY 2006 VL 3 IS 2 BP 149 EP 157 DI 10.2174/156720206776875894 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 052RO UT WOS:000238251300008 PM 16719797 ER PT J AU Miniscalco, C Nygren, G Hagberg, B Kadesjo, B Gillberg, C AF Miniscalco, C Nygren, G Hagberg, B Kadesjo, B Gillberg, C TI Neuropsychiatric and neurodevelopmental outcome of children at age 6 and 7 years who screened positive for language problems at 30 months SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID OF-THE-LITERATURE; KINDERGARTEN-CHILDREN; PRIMARY SPEECH; FOLLOW-UP; PREVALENCE; DISORDERS; SCHOOL; DELAY; DISABILITY; HACKNEY AB We present a prospective study at school age of neuropsychiatric and neurodevelopmental outcome of language delay suspected at child health screening around 30 months of age. In a community sample, 25 children (21 males, 4 females) screening positive and 80 children (38 males, 42 females) screening negative for speech and language problems at age 30 months were examined in detail for language disorders at age 6 years. The screen-positive children were then followed for another year and underwent in-depth neuropsychiatric examination by assessors blind to the results of previous testing. Detailed follow-up results at age 7 years were available for 21 children. Thirteen of these 21 children (62%) had a major neuropsychiatric diagnosis (autism, atypical autism, Asperger's syndrome, attention-deficit-hyperactivity disorder [ADHD]), or combinations of these. Two further children (10%) had borderline IQ with no other major diagnosis. We conclude that children in the general population who screen positive for speech and language problems before age 3 years appear to be at very high risk of autism spectrum disorders or ADHD, or both, at 7 years of age. 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Med. Child Neurol. PD MAY PY 2006 VL 48 IS 5 BP 361 EP 366 DI 10.1017/S0012162206000788 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 037UV UT WOS:000237173900009 PM 16608544 ER PT J AU McIntosh, DN Reichmann-Decker, A Winkielman, P Wilbarger, JL AF McIntosh, DN Reichmann-Decker, A Winkielman, P Wilbarger, JL TI When the social mirror breaks: deficits in automatic, but not voluntary, mimicry of emotional facial expressions in autism SO DEVELOPMENTAL SCIENCE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; IMITATION; CHILDREN; PERCEPTION; MECHANISMS; RESPONSES; SPECTRUM AB Humans, infants and adults alike, automatically mimic a variety of behaviors. Such mimicry facilitates social functioning, including establishment of interpersonal rapport and understanding of other minds. This fundamental social process may thus be impaired in disorders such as autism characterized by socio-emotional and communicative deficits. We examined automatic and voluntary mimicry of emotional facial expression among adolescents and adults with autistic spectrum disorders (ASD) and a typical sample matched on age, gender and verbal intelligence. Participants viewed pictures of happy and angry expressions while the activity over their cheek and brow muscle region was monitored with electromyography (EMG). ASD participants did not automatically mimic facial expressions whereas the typically developing participants did. However, both groups showed evidence of successful voluntary mimicry. The data suggest that autism is associated with an impairment of a basic automatic social-emotion process. Results have implications for understanding typical and atypical social cognition. C1 Univ Denver, Dept Psychol, Denver, CO 80208 USA. Univ Calif San Diego, Dept Psychol, San Diego, CA 92103 USA. Univ Wisconsin, Dept Kinesiol, Madison, WI USA. 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TI A case of pervasive developmental disorder with chromosomal translocation (X;4) (p11;q13) SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE chromosome; pervasive developmental disorder; translocation ID AUTISM AB Introduction. Chromosomal aberrations, with or without congenital physical abnormalities, have, been frequently found associated with neuropsychiatric disorders, including mental retardation, psychosis, autism, and criminal behaviour. The meaning of the association frequently remains unclear. However, consistent, findings of association between specific chromosomal abnormalities and clinical phenotype may. provide evidence,:of a causal relationship and shed light on the pathogenesis of obscure disorders. Case-report. Here, we present the case of a 28-year-old, Caucasian male affected by pervasive developmental disorder, associated with chromosomal translocation 46, XY, t,(X; 4) (p11; q13), and abnormal facial features. A few days after birth, the patient was taken a Way from his parents and adopted for.. unknown reasons. No information is available about his biological relatives Mild delay in the development of spoken language was reported. Since early childhood, the patient's behaviour was characterized by troublesome relationship with his parents and his fellows, and persistent violation of norms and rules at home and at school. Consequently, social and school functioning was poor. When he was eight, verbal and motor stereotypy appeared for the first time. As an adolescent, he was more and more aggressive. He exhibited countless episodes of rage and verbal and physical aggressiveness. After he had completed secondary school, his way of life was chaotic. He got into the habit of staying away from home; sleeping in the day and vagabonding at night He began to abuse alcohol. Grandiosity and persecutory delusions became evident. He claimed to hate the Vatican, the Pope, and the Polish people and to be the Devil, the Antichrist He feared that his food was poisoned by his mother and-refused to eat at home any more. He loved to remain in a cage with two wild dogs, accumulating and keeping bottles full of his urine. He often engaged in violent fights in the street with tramps and foreigners. Finally, he was involuntary admitted to a psychiatric intensive care unit. He, was hostile, uncooperative, and violent Magnetic resonance imaging of brain was normal, Wechsler Adult Intelligence-Scale IQ score was 96 (total), 108 (verbal), 80 (non verbal), and Standard Progressive Matrices score was 44160, chromosomal examination [banding R (RBG)] revealed\ an apparently balanced translocation 46, XY, t (X; 4) (p11; q13). The patient was treated with risperidone (8 mg/day) and valproate (1500 2000 mg/day) with improvement Psychotic symptoms, hostility and violence vanished. Amazingly, his behaviour and attitude,became normal. Very early onset of symptoms, absence of negative signs, and dysmorphic features suggesting an underlying medical disease do not support the diagnosis of schizophrenia. Discussion. The diagnosis of pervasive developmental disorder, not otherwise specified, could be made, considering the delay in the development of spoken language, the large discordance between verbal and non verbal WAIS IQ score, the presence, of stereotypy, abnormal facial features, and motor clumsiness. The late onset of symptoms precludes the diagnosis of autism, while the delay in language does not permit the diagnosis of Asperger's disorder. The lack of information on his biological relatives did not permit us to assess the presence of genetic, physical or mental abnormalities in his family. Therefore, the causal relationship between the chromosomal translocation and the psychiatric disorder is uncertain in this patient. Similar genetic abnormalities found in atients affected by neuropsychiatric, disorders could confirm an etiological link. C1 Hop S Spirito Sassia, Psychiat Serv, Rome, Italy. RP Azzoni, A (reprint author), Hop S Spirito Sassia, Psychiat Serv, Rome, Italy. CR Auranen M, 2000, MOL PSYCHIATR, V5, P320, DOI 10.1038/sj.mp.4000708 Nasr A, 2000, J INTELL DISABIL RES, V44, P170, DOI 10.1046/j.1365-2788.2000.00239.x Raja M, 2001, GEN HOSP PSYCHIAT, V23, P285, DOI 10.1016/S0163-8343(01)00155-4 Ramanathan Subhadra, 2004, BMC Med Genet, V5, P10, DOI 10.1186/1471-2350-5-10 Sabaratnam M, 2000, EUR CHILD ADOLES PSY, V9, P307 NR 5 TC 0 Z9 0 PU MASSON EDITEUR PI MOULINEAUX CEDEX 9 PA 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE SN 0013-7006 J9 ENCEPHALE JI Enceph.-Rev. Psychiatr. Clin. Biol. Ther. 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Brachydactyly is a variable but characteristic feature of this clinical entity. Here we report on five cases of cytogenetically visible de novo deletions of this 2q37 chromosome region. Using FISH, we characterized at the molecular level the breakpoints of these deletions using a set of 15 BACs, PACs and YACs. In four patients, terminal deletions of variable size ranged between 6.2 and 10 Mb. The fifth patient had an interstitial deletion with an AHO-like phenotype including brachydactyly. These findings when compared to previous observations allowed us to narrow down the brachydactyly critical region between BACs RP11-585E12 and RP11-351810. It contains HDAC4 and STK25 candidate genes loci. (c) 2005 Elsevier SAS. All rights reserved. C1 Hop Necker Enfants Malad, Dept Genet, F-75743 Paris 15, France. Fac Med Tunis, Dept Genet, Tunis, Tunisia. RP Romana, SP (reprint author), Hop Necker Enfants Malad, Dept Genet, 149 Rue Sevres, F-75743 Paris 15, France. 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In the adult motor cortex, performing actions and observing human movement reduces the magnitude of the mu (8-13 Hz) rhythm, possibly reflecting MN system activity. Despite the wealth of information available regarding the adult MN system, little is known about its existence in children. Here, we used EEG to probe mu rhythm modulation in 15 children during observation and execution of hand actions. Our data show that mu rhythm attenuation occurs in children under 11 years old during observation of hand movements. Similarly to what has been reported in adults, observation of goal/object-orientated movement produces greater modulation of the mu rhythm than intransitive movement. These data confirm the existence of an observation-execution matching system in the immature human brain and may be of clinical value in the understanding of neurodevelopmental disorders associated with a faulty MN system, such as autism spectrum disorder. 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The aim of this study was to establish the carer-reported prevalence of social, communication, and behavioural problems in middle childhood in a total population with neuromuscular diseases. From a target population of 111, 82 carers of children aged 5-13 years with a diagnosed neuromuscular disease living in the Northern Region of UK were interviewed about service utilisation and needs, and 66 completed the Strengths and Difficulties Questionnaire, Social Communication Questionnaire and Children's Communication Checklist. Two-fifths of children scored above the clinical cut-off on at least one questionnaire. These results were significantly higher than are reported for national and normally developing samples. Nine out of 82 had a diagnosis of autism spectrum disorder. Carers of children with problems reported significantly higher levels of unmet need. Behaviour, social and communication problems are common in children with neuromuscular diseases and Regional Neuromuscular Clinics should consider mental health screening and assessment. (C) 2006 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved. C1 Univ Newcastle Upon Tyne, Royal Victoria Infirm, Sch Clin Med Sci, Sir James Spence Inst, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England. Univ Newcastle Upon Tyne, Sch Med, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. Univ Newcastle Upon Tyne, Inst Human Genet, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. RP McConachie, H (reprint author), Univ Newcastle Upon Tyne, Royal Victoria Infirm, Sch Clin Med Sci, Sir James Spence Inst, Queen Victoria Rd, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England. 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It has sometimes been assumed in the literature that deviations in regional brain size in clinical samples are directly related to maldevelopment or pathogenesis. However, this assumption may be incorrect; such volume differences may, instead, be wholly or partly attributable to individual differences in overall dimension (e.g., for head, brain, or body size). What quantitative approaches can be used to take these factors into account? Here, we provide a review of volumetric and nonvolumetric adjustment factors. We consider three examples of common statistical methods by which one can adjust for the effects of body, head, or brain size on regional volumetric measures: the analysis of covariance, the proportion, and the residual approaches. 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Rev. Psychiatr. PD MAY-JUN PY 2006 VL 14 IS 3 BP 141 EP 151 DI 10.1080/10673220600784119 PG 11 WC Psychiatry SC Psychiatry GA 058XH UT WOS:000238697400002 PM 16787886 ER PT J AU Seth, R Kalra, V AF Seth, R Kalra, V TI Autism in India SO INDIAN PEDIATRICS LA English DT Letter C1 All India Inst Med Sci, Dept Pediat, New Delhi 110029, India. RP Seth, R (reprint author), All India Inst Med Sci, Dept Pediat, New Delhi 110029, India. EM kalra_veena@hotmail.com CR Juneja M, 2005, INDIAN PEDIATR, V42, P453 Kalra Veena, 2005, Indian Journal of Pediatrics, V72, P227, DOI 10.1007/BF02859263 Singhi P, 2001, Indian Pediatr, V38, P384 NR 3 TC 0 Z9 0 PU INDIAN ACADEMY PEDIATRICS PI NEW DELHI PA MAULANA AZAD MEDICAL COLLEGE, DEPT PEDIATRICS, NEW DELHI, 110 002, INDIA SN 0019-6061 J9 INDIAN PEDIATR JI Indian Pediatrics PD MAY PY 2006 VL 43 IS 5 BP 456 EP 456 PG 1 WC Pediatrics SC Pediatrics GA 044XJ UT WOS:000237706600017 PM 16735776 ER PT J AU Caldwell, P AF Caldwell, Phoebe TI Speaking the other's language: imitation as a egateway to relationship SO INFANT AND CHILD DEVELOPMENT LA English DT Article; Proceedings Paper CT Conference on Imitation and Socio-Emotional Process - Implications for Communicative Development Interventions CY 2004 CL Leeds, ENGLAND DE imitation; autism; intensive interaction; engagement; infancy; social interaction AB Imitation offers a gateway to relationship. This paper seeks to explore that capacity by describing the therapeutic approach of 'Intensive Interaction'. The research literature on imitation contains relatively little about imitation used in an intervention capacity, concentrating instead on the emergence of imitative abilities during infant and child development. The paper therefore describes the case of a young man with severe autism, for whom Intensive Interaction was successful in bringing him into interpersonal engagement with others. The author provides an account as to why imitation should be so effective in this regard. Overall, the paper aims to stimulate questions about how imitation can best be conceived and studied. Copyright (c) 2006 John Wiley & Sons, Ltd. RP Caldwell, P (reprint author), Beechstones Barn, Lancaster LA2 7LA, England. 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PD MAY-JUN PY 2006 VL 15 IS 3 BP 275 EP 282 DI 10.1002/icd.456 PG 8 WC Psychology, Developmental SC Psychology GA 060DA UT WOS:000238780900006 ER PT J AU Heimann, M Laberg, KE Nordoen, B AF Heimann, Mikael Laberg, Kari E. Nordoen, Bodil TI Imitative interaction increases social interest and elicited imitation in non-verbal children with autism SO INFANT AND CHILD DEVELOPMENT LA English DT Article; Proceedings Paper CT Conference on Imitation and Socio-Emotional Process - Implications for Communicative Development Interventions CY 2004 CL Leeds, ENGLAND DE autism; imitation; social interest ID TO-FACE INTERACTION; DEFICITS AB Recent studies indicate that being intensely imitated for a brief period of time increases social interest among children with autism. The aim of this study was to replicate and extend these findings. Twenty children with an autism spectrum disorder (ASD) were randomly assigned to one of two interaction strategies: imitation (n = 10) or contingent (n = 10). The children had little or no functional speech, and their developmental age averaged 25 months (mean chronological age =6:5 years). Both conditions were presented with repeated sessions of a modified version of Nadel's 'still-face' paradigm (still-face/intervention/still-face/spontaneous play). The analysis revealed a significant increase of both proximal and distal social behaviours (touch and look at person) for the imitation condition, which confirms previous reports. In addition, an increase in elicited imitation, as measured with the PEP-R developmental assessment procedure, was also observed for children in the imitation condition, but not in the contingent condition. This finding extends earlier reports in that it suggests that the social expectancies unlocked by imitation also spread to tasks outside the experimental setting. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Univ Bergen, N-5020 Bergen, Norway. Eikelund Resource Ctr, Bergen, Norway. 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PD MAY-JUN PY 2006 VL 15 IS 3 BP 297 EP 309 DI 10.1002/icd.463 PG 13 WC Psychology, Developmental SC Psychology GA 060DA UT WOS:000238780900008 ER PT J AU Persson, C Niklasson, L Oskarsdottir, S Johansson, S Jonsson, R Soderpalm, E AF Persson, C Niklasson, L Oskarsdottir, S Johansson, S Jonsson, R Soderpalm, E TI Language skills in 5-8-year-old children with 22q11 deletion syndrome SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE 22q11 deletion syndrome; language impairment; narrative analysis; phonology; receptive vocabulary ID CARDIO-FACIAL SYNDROME; VELOCARDIOFACIAL-SYNDROME; CHROMOSOME 22Q11; FOLLOW-UP; SPEECH; DISORDERS; MICRODELETION; ADOLESCENCE; 4-YEAR-OLDS; PROFILES AB Background: Language impairment and delayed language onset have been described, although not investigated in detail, in children with 22q11 deletion syndrome. Aims: To investigate different areas of language: the ability to retell a narrative, phonology, syntax and receptive vocabulary in a group of 5-8-year-old children with 22q11 deletion syndrome regardless of whether or not they had a history of speech and language difficulties. Gender differences were also investigated. Methods & Procedures: Nineteen consecutively referred children with 22q11 deletion syndrome, ten girls and nine boys, between the ages of 5 and 8 v-ears, participated in the study. The mean full-scale IQ of the group was 78. Six children had an autism spectrum disorder, attention deficit/hyperactivity disorder, or a combination of these. Three different language tests were used: (1) the Bus Story - a test of narrative speech and language; (2) an articulation test including all Swedish phonemes in different positions; and (3) the Peabody Picture Vocabulary Test - Revised (PPVT-R). Outcomes &.Results: All but two children had an information score in the retelling task of 1 SD below the population mean. A negative correlation between age and the information score implied that the older the children, the more severe the problems. One child had an average sentence length within the normal limits and five children had subordinate clauses within normal limits. A median of 4% of the utterances included grammatical errors. About 50% of the children had a complete consonant inventory. The phonological process analysis implied delayed rather than deviant development. The group had a moderately low score for receptive vocabulary. Conclusions: Language difficulties in all investigated areas of language were found. It is suggested that speech-language impairment is a common feature of 22q11 deletion syndrome. 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J. Lang. Commun. Disord. PD MAY-JUN PY 2006 VL 41 IS 3 BP 313 EP 333 DI 10.1080/13682820500361497 PG 21 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 047ML UT WOS:000237883300005 PM 16702096 ER PT J AU Reynhout, G Carter, M AF Reynhout, G Carter, M TI Social Stories (TM) for children with disabilities SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Social Stories (TM); autism; Asperger's syndrome; behavior modification; social skills; special education ID SINGLE-SUBJECT RESEARCH; QUANTITATIVE SYNTHESIS; ASPERGER-SYNDROME; AUTISM; INTERVENTION; STUDENTS; METAANALYSIS; BEHAVIORS; VALIDITY; SKILLS AB A review of the empirical research literature on Social Stories (TM) is presented, including a descriptive review and single-subject meta-analysis of appropriate studies. Examination of data suggests the effects of Social Stories (TM) are highly variable. Interpretations of extant studies are frequently confounded by inadequate participant description and the use of Social Stories (TM) in combination with other interventions. It is unclear whether particular components of Social Stories (TM) are central to their efficacy. Data on maintenance and generalization are also limited. Social Stories (TM) stand as a promising intervention, being relatively straightforward and efficient to implement with application to a wide range of behaviors. Further research is needed to determine the exact nature of their contribution and the components critical to their efficacy. C1 Macquarie Univ, Sepcial Educ Ctr, N Ryde, NSW 2109, Australia. RP Reynhout, G (reprint author), Macquarie Univ, Sepcial Educ Ctr, N Ryde, NSW 2109, Australia. EM reynhout@speced.sed.mq.edu.au CR Alberto P. 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PD MAY PY 2006 VL 36 IS 4 BP 445 EP 469 DI 10.1007/s10803-006-0086-1 PG 25 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600002 PM 16755384 ER PT J AU Mandell, DS Cao, J Ittenbach, R Pinto-Martin, J AF Mandell, DS Cao, J Ittenbach, R Pinto-Martin, J TI Medicaid expenditures for children with autistic spectrum disorders: 1994 to 1999 SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; medicaid; healthcare costs ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGERS-DISORDER; MENTAL-RETARDATION; PEDIATRICIANS ROLE; SERVICE DELIVERY; HEALTH-SERVICES; US CHILDREN; CARE; DIAGNOSIS; CLAIMS AB This study used data from 1994 to 1999 from one large county in Pennsylvania to estimate the Medicaid expenditures of children diagnosed with autism spectrum disorders (ASD) and to compare these expenditures with those of other Medicaid-eligible children. On average, children diagnosed with ASD had expenditures 10 times those of other children. Differences in expenditures were driven in large part by inpatient psychiatric care. Further research is required to determine whether hospitalized children could be served in less restrictive and less expensive settings. Lack of differences in ambulatory care expenditures suggests that children with ASD are not receiving additional primary care services that would be indicative of appropriately coordinated services as suggested by the medical home model. C1 Univ Penn, Sch Med, Dept Psychiat, Hlth Syst,Ctr Mental Hlth Policy & Serv Res, Philadelphia, PA 19104 USA. Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA. Temple Univ, Dept Stat, Philadelphia, PA 19122 USA. Childrens Hosp, Div Biostat, Philadelphia, PA 19104 USA. Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA. RP Mandell, DS (reprint author), Univ Penn, Sch Med, Dept Psychiat, Hlth Syst,Ctr Mental Hlth Policy & Serv Res, 3535 Market St,3rd Floor, Philadelphia, PA 19104 USA. 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Autism Dev. Disord. PD MAY PY 2006 VL 36 IS 4 BP 475 EP 485 DI 10.1007/s10803-006-0088-z PG 11 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600004 PM 16586155 ER PT J AU Ingersoll, B Schreibman, L AF Ingersoll, B Schreibman, L TI Teaching reciprocal imitation skills to young children with autism using a naturalistic behavioral approach: Effects on language, pretend play, and joint attention SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; imitation; intervention; behavioral; social communication ID SCHIZOPHRENIC CHILDREN; SYMBOLIC PLAY; COMMUNICATION; DELAY; SPECTRUM; DESIGNS; OBJECT AB Children with autism exhibit significant deficits in imitation skills which impede the acquisition of more complex behaviors and socialization, and are thus an important focus of early intervention programs for children with autism. 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Autism Dev. Disord. PD MAY PY 2006 VL 36 IS 4 BP 487 EP 505 DI 10.1007/s10803-006-0089-y PG 19 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600005 PM 16568355 ER PT J AU Ludlow, AK Wilkins, AJ Heaton, P AF Ludlow, AK Wilkins, AJ Heaton, P TI The effect of coloured overlays on reading ability in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; colour perception; reading; academic achievement; coloured overlays ID VISUAL DISCOMFORT; INFANTILE-AUTISM; MIGRAINE; POPULATION; EPIDEMIOLOGY; CLASSROOM; EPILEPSY; FILTERS; LENSES; TRIAL AB Abnormalities of colour perception in children with autistic spectrum disorders have been widely reported anecdotally. However, there is little empirical data linking difficulties in colour perception with academic achievement. The Wilkins Rate of Reading Test was administered with and without Intuitive Coloured Overlays to 19 children with autistic spectrum disorders and to the same number of controls individually matched for age and intelligence. Findings showed that 15 out of 19 (79%) children with autism showed an improvement of at least 5% in reading speed when using a coloured overlay. In contrast only 3 of 19 (16%) control group children showed such an improvement. The findings suggest that coloured overlays may provide a useful support for reading for children with autism. C1 Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. Univ Essex, Dept Psychol, Colchester CO4 3SQ, Essex, England. RP Ludlow, AK (reprint author), Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. EM ps901akl@gold.ac.uk CR [Anonymous], 1994, DIAGNOSTIC STAT MANU Aurora SK, 1998, CURR OPIN NEUROL, V11, P205, DOI 10.1097/00019052-199806000-00003 BARTAK L, 1975, COGNITIVE DEFICITS R BOULDOUKIAN J, 2002, OPHTHAL PHYSL OPT, V221, P55 *BRIT PSYCH SOC, 1999, REP WORK PART DIV ED BRYSON SE, 1988, J CHILD PSYCHOL PSYC, V29, P433, DOI 10.1111/j.1469-7610.1988.tb00735.x CHRONICLE EP, 1995, CEPHALALGIA, V15, P117, DOI 10.1046/j.1468-2982.1995.015002117.x CHRONICLE EP, 1991, LANCET, V338, P890, DOI 10.1016/0140-6736(91)91549-A CIALDELLA P, 1989, J CHILD PSYCHOL PSYC, V30, P165, DOI 10.1111/j.1469-7610.1989.tb00775.x CORBETT J, 1982, HDB PSYCHIAT, P198 CROBRINIK L, 1974, J AUTISM CHILD SCHIZ, V4, P163 DEYKIN EY, 1979, AM J PSYCHIAT, V136, P1310 DUNN LI, 1997, BRIT PICTURE VOCABLU Evans B. J. 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J., 2003, READING COLOUR WILKINS AJ, 1987, ERGONOMICS, V30, P1705, DOI 10.1080/00140138708966059 Wilkins AJ, 1995, VISUAL STRESS Wilkins AJ, 1996, OPHTHAL PHYSL OPT, V16, P491, DOI 10.1016/0275-5408(96)00028-2 WILKINS AJ, 1994, OPHTHAL PHYSL OPT, V14, P365, DOI 10.1111/j.1475-1313.1994.tb00126.x Wilkins AJ, 2002, CEPHALALGIA, V22, P711, DOI 10.1046/j.1468-2982.2002.00362.x Wilkins Arnold. J., 2001, J RES READ, V181, P10 WILLIAMS D, 1999, LIKE COLOUR BLIND WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Xiao YP, 2003, NATURE, V421, P535, DOI 10.1038/nature01372 NR 53 TC 15 Z9 15 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD MAY PY 2006 VL 36 IS 4 BP 507 EP 516 DI 10.1007/s10803-006-0090-5 PG 10 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600006 PM 16598434 ER PT J AU Kylliainen, A Hietanen, JK AF Kylliainen, A Hietanen, JK TI Skin conductance responses to another person's gaze in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high functioning autism; skin conductance responses; electrodermal activity; eye contact; gaze direction ID EYE CONTACT; AUTONOMIC RESPONSES; INFANT SENSITIVITY; BEHAVIOR; PERCEPTION; ATTENTION; STIMULI; DIRECTION; LOOKING; INDIVIDUALS AB The effects of another person's gaze on physiological arousal were investigated by measuring skin conductance responses (SCR). Twelve able children with autism and 12 control children were shown face stimuli with straight gaze (eye contact) or averted gaze on a computer monitor. In children with autism, the responses to straight gaze were stronger than responses to averted gaze, whereas there was no difference in the responses to these gaze conditions in normally developing children. Thus, these results showed that eye gaze elicited differential pattern of SCR in normally developing children and in children with autism. It is possible that the enhanced arousal to eye contact may contribute to the abnormal gaze behaviour frequently reported in the context of autism. C1 Univ Tampere, Dept Psychol, FIN-33101 Tampere, Finland. RP Kylliainen, A (reprint author), Univ Tampere, Dept Psychol, FIN-33101 Tampere, Finland. EM anneli.kylliainen@uta.fi CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Andreassi J. 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PD MAY PY 2006 VL 36 IS 4 BP 517 EP 525 DI 10.1007/s10803-006-0091-4 PG 9 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600007 PM 16555137 ER PT J AU Zalla, T Labruyere, N Georgieff, N AF Zalla, Tiziana Labruyere, Nelly Georgieff, Nicolas TI Goal-directed action representation in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE action knowledge; sequencing errors; goal detection ID FRONTAL-LOBE DAMAGE; PREFRONTAL CORTEX DAMAGE; HIGH-FUNCTIONING AUTISM; CHILDHOOD AUTISM; CHILDREN; MIND; PERCEPTION; INTENTIONS; BEHAVIOR; IMPAIRMENTS AB The aim of the present study was to investigate the ability of individuals with autism to represent goal-directed behavioural actions. We compared the performance of subjects with autism (n=16), mentally retarded subjects (n=14) and normal healthy subjects (n=15) in a sequencing task consisted in arranging pictures of single events in their appropriate order so as to make coherent stories. Three types of actions were presented: (a) actions on objects; (b) actions on objects in a broader spatio-temporal context; (c) interactive actions. Autistic subjects were impaired in arranging sequences of actions on objects, as compared to both control groups. This impairment might contribute to explaining both executive deficits and difficulties in understanding others' behaviour in autism. C1 Inst Cognit Sci, Bron, France. RP Zalla, T (reprint author), Inst Jean Nicod, 1bis,Ave Lowendal, F-75007 Paris, France. 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PD MAY PY 2006 VL 36 IS 4 BP 527 EP 540 DI 10.1007/s10803-006-0092-3 PG 14 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600008 PM 16568354 ER PT J AU Martin, SC Wolters, PL Smith, ACM AF Martin, SC Wolters, PL Smith, ACM TI Adaptive and maladaptive behavior in children with Smith-Magenis syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Smith-Magenis syndrome; adaptive functioning; social skills; IQ ID INTELLIGENCE SCALE; SEX-DIFFERENCES; SELF-INJURY; AUTISM; RELIABILITY; PROFILES; VALIDITY; DELETION; COMORBIDITY; PHENOTYPE AB Children with Smith-Magenis Syndrome (SMS) exhibit deficits in adaptive behavior but systematic studies using objective measures are lacking. This descriptive study assessed adaptive functioning in 19 children with SMS using the Vineland Adaptive Behavior Scales (VABS). Maladaptive behavior was examined through parent questionnaires and the Childhood Autism Rating Scale. Cognitive functioning was evaluated with an age-appropriate test. Children scored below average on VABS Communication, Daily Living Skills, and Socialization scales. Learning problems and hyperactivity scales on the Conner's Parent Rating Scale were elevated, and girls were more impulsive than boys. Stereotypic and self-injurious behaviors were present in all children. Cognitive functioning was delayed and consistent with communication and daily living skills, while socialization scores were higher than IQ. C1 NCI, HIV & AIDS Malignancy Branch, Bethesda, MD 20892 USA. Med Illness Counseling Ctr, Chevy Chase, MD USA. NHGRI, Med Genet Branch, Bethesda, MD 20892 USA. RP Martin, SC (reprint author), NCI, HIV & AIDS Malignancy Branch, 9030 Old Georgetown Rd 107, Bethesda, MD 20892 USA. EM martins@mail.nih.gov CR Achenbach T. 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Autism Dev. Disord. PD MAY PY 2006 VL 36 IS 4 BP 541 EP 552 DI 10.1007/s10803-006-0093-2 PG 12 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600009 PM 16570214 ER PT J AU Kunihira, Y Senju, A Dairoku, H Wakabayashi, A Hasegawa, T AF Kunihira, Y Senju, A Dairoku, H Wakabayashi, A Hasegawa, T TI 'Autistic' traits in non-autistic japanese populations: Relationships with personality traits and cognitive ability SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism-Spectrum Quotient (AQ); general population; personality; depression; anxiety; cognitive ability ID OBSESSIVE-COMPULSIVE DISORDER; HIGH-FUNCTIONING CHILDREN; WEAK CENTRAL COHERENCE; ASPERGER-SYNDROME; EXECUTIVE FUNCTION; FAMILY HISTORY; MIND; PHENOTYPE; PARENTS; ADULTS AB We explored the relationships between 'autistic' traits as measured by the AQ (Autism-Spectrum Quotient; Baron-Cohen et al., J. Autism Develop. Disord. (2001b) 31 5) and various personality traits or cognitive ability, which usually coincide with autistic symptoms, for general populations. Results showed the AQ was associated with tendencies toward an obsessional personality as defined by the TCI (Temperament and Character Inventory), higher depression and anxiety, and higher frequency of experience of being bullied. These results parallel the patterns in autism and corroborate the validity of the AQ for general populations. Contrary to our prediction, however, there was no relationship between the AQ and cognitive ability, such as theory of mind, executive functioning, and central coherence, suggesting the AQ does not reflect autism-specific cognitive patterns in general populations. C1 Univ Tokyo, Meguro Ku, Dept Cognit & Behav Sci, Meguro Ku, Tokyo 1538902, Japan. Univ London, Dept Psychol, Ctr Brain & Cognit Dev, London, England. Musashino Univ, Fac Human Studies, Tokyo, Japan. Univ Tsukuba, Inst Disabil Sci, Ibaraki, Japan. Chiba Univ, Fac Letters, Chiba, Japan. RP Kunihira, Y (reprint author), Univ Tokyo, Meguro Ku, Dept Cognit & Behav Sci, Meguro Ku, 3-8-1 Komaba, Tokyo 1538902, Japan. 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D., 1970, MANUAL STATE TRAIT TAKUMA T, 2001, FUTAGO KENKYU TANNO Y, 1994, UNPUB RES BULLED BUL Volkmar F, 1999, J AUTISM DEV DISORD, V29, P185, DOI 10.1023/A:1023009230857 VREDENBURG K, 1993, PSYCHOL BULL, V113, P327, DOI 10.1037/0033-2909.113.2.327 Wakabayashi A., 2003, JAPANESE J AUTISTIC, V2, P11 WAKABAYASHI A, UNPUB AUTISM SPECTRU Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 WING L, 1981, PSYCHOL MED, V11, P115 Witkin HA, 1971, MANUAL EMBEDDED FIGU World Health Organization, 1994, INT CLASS DIS ZUNG WWK, 1965, ARCH GEN PSYCHIAT, V12, P63 NR 55 TC 39 Z9 39 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD MAY PY 2006 VL 36 IS 4 BP 553 EP 566 DI 10.1007/s10803-006-0094-1 PG 14 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600010 PM 16602034 ER PT J AU Gevers, C Clifford, P Mager, M Boer, F AF Gevers, C Clifford, P Mager, M Boer, F TI Brief report: A theory-of-mind-based social-cognition training program for school-aged children with pervasive developmental disorders: An open study of its effectiveness SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID AUTISM; PERFORMANCE; ABILITIES; BELIEFS C1 AMC, Dept Child & Adolescent Psychiat, NL-1100 AL Amsterdam, Netherlands. Acad Ctr Child & Adolescent Psychiat, Amsterdam, Netherlands. RP Gevers, C (reprint author), AMC, Dept Child Adol Psychiat Bascule, POB 12474, NL-1100 AL Amsterdam, Netherlands. EM c.gevers@debascule.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S, 1997, HDB AUTISM PERVASIVE, P880 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x Buitelaar JK, 1999, J CHILD PSYCHOL PSYC, V40, P869, DOI 10.1017/S0021963099004321 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x Muris P, 1999, J AUTISM DEV DISORD, V29, P67, DOI 10.1023/A:1025922717020 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 PERNER J, 1985, J EXP CHILD PSYCHOL, V39, P437, DOI 10.1016/0022-0965(85)90051-7 PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x Serra M, 2002, J CHILD PSYCHOL PSYC, V43, P885, DOI 10.1111/1469-7610.00104 SERRA M, 1995, J CHILD PSYCHOL PSYC, V36, P475, DOI 10.1111/j.1469-7610.1995.tb01304.x Sparrow S, 1984, VINELAND ADAPTIVE BE Steele S, 2003, J AUTISM DEV DISORD, V33, P461, DOI 10.1023/A:1025075115100 Steememan P., 1996, CLIN CHILD PSYCHOL P, V1, P251, DOI 10.1177/1359104596012006 Steerneman P., 2000, TOM TEST Wechsler D, 1974, WECHSLER INTELLIGENC WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 NR 21 TC 14 Z9 14 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD MAY PY 2006 VL 36 IS 4 BP 567 EP 571 DI 10.1007/s10803-006-0095-0 PG 5 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600011 PM 16586154 ER PT J AU Fitzgerald, M Bellgrove, MA AF Fitzgerald, M Bellgrove, MA TI The overlap between alexithymia and Asperger's syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID SEROTONIN TRANSPORTER; FUNCTIONING AUTISM; DISORDER; PATIENT C1 Univ Dublin Trinity Coll, Dept Psychiat, Dublin 2, Ireland. Univ Dublin Trinity Coll, Dept Psychol, Dublin 2, Ireland. Univ Dublin Trinity Coll, Inst Neurosci, Dublin 2, Ireland. RP Fitzgerald, M (reprint author), Univ Dublin Trinity Coll, Dept Psychiat, Dublin 2, Ireland. EM fitzi@iol.ie CR Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Cook EH, 1997, MOL PSYCHIATR, V2, P247 DAMASIO AR, 1978, ARCH NEUROLOGY, V35 Egan MF, 2001, P NATL ACAD SCI USA, V98, P6917, DOI 10.1073/pnas.111134598 FREYBERGER H, 1977, THEORY PSYCHOMATIC D FREYBERGER H, HOWELS MODERN PERSPE Ham BJ, 2005, NEUROPSYCHOBIOLOGY, V52, P151, DOI 10.1159/000087846 Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 HERMELIN B, 1967, BRIT J PSYCHOL, P58 HOPPE KD, 1977, PSYCHOANAL QUART, V46, P220 Kim SJ, 2002, MOL PSYCHIATR, V7, P278, DOI 10.1038/sj/mp/4001033 Klin A., 2000, ASPERGERS SYNDROME KLIN A, 2000, TREATMENT INTERVENTI Krystal H, 1998, INTEGRATION SELF HEA MARTY P, 1963, REV FRANCAISE PSYC S, V27 MCDOUGALL J, 1978, CONTEMP PSYCHOANAL, V14, P173 MCDOUGALL J, 1984, PSYCHOANAL QUART, V53, P386 MCDOUGALL J, 1982, INT J PSYCHOANALYTIC, V9, P377 Nemiah JC, 1996, PSYCHOSOM MED, V58, P217 NEMIAH JC, 1977, PSYCHOTHER PSYCHOSOM, V28, P199 Ogai Masahiro, 2003, Neuroreport, V14, P559, DOI 10.1097/00001756-200303240-00006 PARKER J, 1997, DISORDERS EFFECT REG ROBERTSON LC, 1988, J NEUROSCI, V8, P3757 Shriberg LD, 2001, J SPEECH LANG HEAR R, V44, P1097, DOI 10.1044/1092-4388(2001/087) *TASK FORC REP AM, 1989, TREATM PSYCH DIS TAYLOR GJ, 1984, CAN J PSYCHIAT, V29, P217 Taylor GJ, 1997, DISORDERS AFFECT REG WING L, 1981, PSYCHOL MED, V11, P115 NR 29 TC 21 Z9 21 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD MAY PY 2006 VL 36 IS 4 BP 573 EP 576 DI 10.1007/s10803-006-0096-z PG 4 WC Psychology, Developmental SC Psychology GA 050PO UT WOS:000238100600012 PM 16755385 ER PT J AU Yirmiya, N Gamliel, I Pilowsky, T Feldman, R Baron-Cohen, S Sigman, M AF Yirmiya, N Gamliel, I Pilowsky, T Feldman, R Baron-Cohen, S Sigman, M TI The development of siblings of children with autism at 4 and 14 months: social engagement, communication, and cognition SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; siblings; still face; synchrony; mother-child interaction; language; nonverbal communication; broad phenotype; joint attention ID TO-FACE INTERACTION; MOTHER-INFANT INTERACTION; WEAK CENTRAL COHERENCE; STILL-FACE; JOINT ATTENTION; MENTAL-RETARDATION; SPECTRUM DISORDER; EARLY RECOGNITION; HOME VIDEOTAPES; FAMILY HISTORY AB Aims: To compare siblings of children with autism (SIBS-A) and siblings of children with typical development (SIBS-TD) at 4 and 14 months of age. Methods: At 4 months, mother-infant interactional synchrony during free play, infant gaze and affect during the still-face paradigm, and infant responsiveness to a name-calling paradigm were examined (n = 21 in each group). At 14 months, verbal and nonverbal communication skills were examined as well as cognition (30 SIBS-A and 31 SIBS-TD). Results: Most SIBS-A were functioning as well as the SIBS-TD at 4 and 14 months of age. However, some differences in early social engagement and later communicative and cognitive skills emerged. Synchrony was weaker in the SIBS-A dyads, but only for infant-led interactions. Infant SIBS-A revealed more neutral affect during the still-face procedure and were less upset by it than was true for the SIBS-TD. A surprising result was that significantly more SIBS-A responded to their name being called by their mothers compared to SIBS-TD. At 14 months, SIBS-A made fewer nonverbal requesting gestures and achieved lower language scores on the Bayley Scale. Six SIBS-A revealed a language delay of 5 months and were responsible for some of the significant differences between SIBS-A and SIBS-TD. Furthermore, infant SIBS-A who showed more neutral affect to the still face and were less able to respond to their name being called by their mothers initiated fewer nonverbal joint attention and requesting behaviors at 14 months, respectively. Discussion: Focused on the genetic liability for the broad phenotype of autism as well as the possible influence of having a sibling with autism. C1 Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. Hebrew Univ Jerusalem, Sch Educ, IL-91905 Jerusalem, Israel. Bar Ilan Univ, Dept Psychol, Ramat Gan, Israel. Bar Ilan Univ, Gonda Brain Sci Ctr, Ramat Gan, Israel. Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 1TN, England. Univ Cambridge, Autism Res Ctr, Dept Psychol, Cambridge CB2 1TN, England. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90024 USA. RP Yirmiya, N (reprint author), Hebrew Univ Jerusalem, Dept Psychol, Mt Scopus, IL-91905 Jerusalem, Israel. 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Child Psychol. Psychiatry PD MAY PY 2006 VL 47 IS 5 BP 511 EP 523 DI 10.1111/j.1469-7610.2005.01528.x PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 031XJ UT WOS:000236738200010 PM 16671934 ER PT J AU Prior, M AF Prior, M TI Autism and blindness: research and reflections SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Book Review CR Pring L., 2005, AUTISM BLINDNESS RES NR 1 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD MAY PY 2006 VL 47 IS 5 BP 533 EP 533 DI 10.1111/j.1469-7610.2006.01548.x PG 1 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 031XJ UT WOS:000236738200014 ER PT J AU Edwards, DJ Chugani, DC Chugani, HT Chehab, J Malian, M Aranda, JV AF Edwards, DJ Chugani, DC Chugani, HT Chehab, J Malian, M Aranda, JV TI Pharmacokinetics of Buspirone in autistic children SO JOURNAL OF CLINICAL PHARMACOLOGY LA English DT Article DE Buspirone; pediatrics; pharmacokinetics; gender; autism ID EXTENDED-RELEASE TABLETS; SEROTONIN SYNTHESIS; GRAPEFRUIT JUICE; ANXIETY DISORDER; PHARMACODYNAMICS; VERAPAMIL; CYCLOSPORINE; DISPOSITION; METABOLITE; MIDAZOLAM AB Buspirone is used to treat generalized anxiety disorder in children and may be useful in developmental disorders in which brain serotonin synthesis is altered. Autistic children (13 boys, 7 girls) were given a single oral dose of 2-5 mg (2-3 years) or 5.0 mg (4-6 years). Blood was collected for 8 hours, and plasma was assayed for buspirone and its metabolite 1-pyrimidinylpiperazine (1-PP). The peak concentration of buspirone averaged 1141 +/- 748 pg/mL with a lime to maximum concentration of 0.8 hours. Half-life was 1.6 +/- 0.3 hours. Peak concentrations of 1-PP were 4.5-fold higher than for buspirone. Girls hod higher peak concentrations (1876 vs 746 pg/mL) for buspirone and a lower peak 1-PP/buspirone concentration ratio. These results suggest that buspirone is rapidly absorbed and eliminated in young children with extensive metabolism to 1-PP. Plasma concentrations with 2.5- to 5.0-mg doses were similar to those observed in older children receiving 7.5- to 15-mg doses. C1 Wayne State Univ, Eugene Applebaum Coll Pharm & Hlth Sci, Dept Pharm Practice, Detroit, MI 48201 USA. Wayne State Univ, Carman & Ann Adams Dept Pediat, Detroit, MI 48201 USA. Wayne State Univ, Sch Med, Dept Neurol, Detroit, MI 48201 USA. Wayne State Univ, Dept Radiol, Detroit, MI 48201 USA. Childrens Hosp Michigan, Div Clin Pharmacol, Detroit, MI 48201 USA. Childrens Hosp Michigan, PET Ctr, Detroit, MI 48201 USA. Childrens Hosp Michigan, Dept Pharm Serv, Detroit, MI 48201 USA. NICHD, Pediat Pharmacol Res Unit Network, Detroit, MI USA. RP Edwards, DJ (reprint author), Wayne State Univ, Eugene Applebaum Coll Pharm & Hlth Sci, Dept Pharm Practice, Detroit, MI 48201 USA. EM dje@wayne.edu CR Allgulander C, 2003, CNS SPECTR, V8, P53 Chandana SR, 2005, INT J DEV NEUROSCI, V23, P171, DOI 10.1016/j.ijdevneu.2004.08.002 Chugani DC, 1999, ANN NEUROL, V45, P287, DOI 10.1002/1531-8249(199903)45:3<287::AID-ANA3>3.0.CO;2-9 DUCHARME MP, 1995, CLIN PHARMACOL THER, V57, P485, DOI 10.1016/0009-9236(95)90032-2 Gaspar P, 2003, NAT REV NEUROSCI, V4, P1002, DOI 10.1038/nrn1256 Gorski JC, 1998, CLIN PHARMACOL THER, V64, P133, DOI 10.1016/S0009-9236(98)90146-1 KATES RE, 1981, CLIN PHARMACOL THER, V30, P44 Kivisto KT, 1999, PHARMACOL TOXICOL, V84, P94 Krecic-Shepard ME, 2000, J CLIN PHARMACOL, V40, P219, DOI 10.1177/00912700022008883 Lamberg TS, 1998, CLIN PHARMACOL THER, V63, P640, DOI 10.1016/S0009-9236(98)90087-X Lilja JJ, 1998, CLIN PHARMACOL THER, V64, P655, DOI 10.1016/S0009-9236(98)90056-X LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Mahmood I, 1999, CLIN PHARMACOKINET, V36, P277, DOI 10.2165/00003088-199936040-00003 Mochon M, 1996, J CLIN PHARMACOL, V36, P580 Paine MF, 2005, DRUG METAB DISPOS, V33, P426, DOI 10.1124/dmd.104.002469 Reed MD, 2001, J CLIN PHARMACOL, V41, P1359, DOI 10.1177/00912700122012832 Sakr A, 2001, J CLIN PHARMACOL, V41, P886, DOI 10.1177/00912700122010681 Sakr A, 2001, J CLIN PHARMACOL, V41, P783, DOI 10.1177/00912700122010582 Salazar DE, 2001, J CLIN PHARMACOL, V41, P1351 NR 19 TC 4 Z9 4 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0091-2700 J9 J CLIN PHARMACOL JI J. Clin. Pharmacol. PD MAY PY 2006 VL 46 IS 5 BP 508 EP 514 DI 10.1177/0091270006286903 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 036GG UT WOS:000237059000002 PM 16638734 ER PT J AU McCleery, JP Tully, L Slevc, LR Schreibman, L AF McCleery, JP Tully, L Slevc, LR Schreibman, L TI Consonant production patterns of young severely language-delayed children with autism SO JOURNAL OF COMMUNICATION DISORDERS LA English DT Article ID MENTALLY-RETARDED SUBJECTS; SPECTRUM DISORDER; PHONOLOGICAL DEVELOPMENT; PRESCHOOL-CHILDREN; EARLY RECOGNITION; HOME VIDEOTAPES; SPEECH; AGE; INTERVENTION; CHILDHOOD AB While much attention has been given to documenting the language skills of verbal children with autism, the basic speech sound development patterns of severely language-impaired children with autism are unknown. Previous research has shown that certain consonants are generally produced earlier in development than other consonants, both in typically developing children and in children with language-learning impairments. While several large studies indicate that children with autism who have strong verbal skills have intact phonological development, there is some evidence that children with autism who are more severely language impaired may have abnormal phonological production. This study documents the speech sound development of non-verbal and minimally verbal children with autism. Prompts were administered for each individual speech sound while spontaneous and imitated sounds were recorded and scored. Results indicate that children with autism show the same general speech sound production patterns as typically developing and language-learning impaired children. Learning outcomes: Individuals who read this manuscript will obtain information regarding: (1) normal phonological development, (2) a comparison of speech sound production of a group of 14 children with a diagnosis of autism spectrum disorder with the production of a group of 10 typically developing children, and (3) comparisons of imitated and spontaneous sound production of the children diagnosed with autism spectrum disorder. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Calif San Diego, Dept Psychol 0109, Autism Res Lab, La Jolla, CA 92093 USA. Univ Calif San Diego, Language Product Lab, Dept Psychol, San Diego, CA 92103 USA. RP McCleery, JP (reprint author), Univ Calif San Diego, Dept Psychol 0109, Autism Res Lab, 9500 Gilman Dr, La Jolla, CA 92093 USA. EM jmccleery@psy.ucsd.edu CR American Psychiatric Association, 2004, DIAGN STAT MAN MENT BAILEY A, 1995, PSYCHOL MED, V25, P63 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARTOLUCCI G, 1977, BRIT J DISORD COMMUN, V12, P137 BARTOLUCCI G, 1976, J AUTISM CHILD SCHIZ, V6, P303, DOI 10.1007/BF01537908 Bayley N., 1969, BAYLEY SCALES INFANT Egel A. 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Commun. Disord. PD MAY-JUN PY 2006 VL 39 IS 3 BP 217 EP 231 DI 10.1016/j.jcomdis.2005.12.002 PG 15 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 044HR UT WOS:000237663500005 PM 16480738 ER PT J AU Potts, M Bellows, B AF Potts, M Bellows, B TI Autism and diet SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH LA English DT Editorial Material C1 Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA. RP Bellows, B (reprint author), 314 Warren Hall, Berkeley, CA 94720 USA. EM bbellows@berkeley.edu CR Courchesne E, 2003, JAMA-J AM MED ASSOC, V290, P337, DOI 10.1001/jama.290.3.337 Lesinskiene Sigita, 2002, Medicina (Kaunas), V38, P412 Newschaffer CJ, 2002, EPIDEMIOL REV, V24, P137, DOI 10.1093/epirev.mxf010 Stokstad E, 2003, SCIENCE, V301, P1454 TANOUE Y, 1989, J AUTISM DEV DISORD, V19, P425, DOI 10.1007/BF02212940 Wakefield A, 2002, MOL PSYCHIATR, V7, pS44, DOI 10.1038/sj.mp.4001178 NR 6 TC 0 Z9 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0143-005X J9 J EPIDEMIOL COMMUN H JI J. Epidemiol. Community Health PD MAY PY 2006 VL 60 IS 5 BP 375 EP 375 DI 10.1136/jech.2005.040261 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 032RO UT WOS:000236792400002 PM 16614324 ER PT J AU Kerr, AM Archer, HL Evans, JC Prescott, RJ Gibbon, F AF Kerr, AM Archer, HL Evans, JC Prescott, RJ Gibbon, F TI People with MECP2 mutation-positive Rett disorder who converse SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; MECP2; Rett; speech; severity ID X-CHROMOSOME INACTIVATION; AUTISM; EXPRESSION; PHENOTYPE; FEATURES; FEMALES; MODEL; GENE AB Background People with useful speech after regression constitute a distinct group of those with mutation-positive Rett disorder, 6% (20/331) reported among mutation-positive people in the British Survey. We aimed to determine the physical, mental and genetic characteristics of this group and to gain insight into their experience of Rett syndrome. Methods Clinical and molecular data for people with Rett, aged 10 or more years at follow-up (the study group, n = 13), with the ability to converse and a MECP2 mutation are presented. They were compared with an age-matched control group (n = 110), who could not converse and had a pathogenic MECP2 mutation. Results The study group differed significantly from the control group with regard to their disease severity (P < 0.001); feeding difficulty scores (P < 0.001); health scores (P < 0.001); epilepsy (P < 0.001); head circumference (P < 0.004); age at onset of the regression period (P < 0.001) (six in the study group did not regress) and mutation frequency (C-terminal deletions P = 0.014, R133C P < 0.006). The results indicate that favourable skewing of X-inactivation is only present in a small proportion of mild cases. Speech was fragmented with a soft, breathless quality, and all but two had obviously irregular breathing. One person with an R168X mutation preferred signing to speech. All enjoyed interpersonal contact, showing affection and preferring people to objects, clearly distinguishing the condition from autism. Most were habitually anxious. Music was a source of pleasure and relaxation also providing a valuable educational asset. Even in these most able cases, understanding was severely restricted in most and little initiative was shown. Conclusions While the Rett profile is present in these people they are commonly not classic, and the presence of speech, good head growth and lack of regression may lead to missed diagnoses. A strong association was demonstrated between this milder form of the disease and R133C and C-terminal deletions. C1 Cardiff Univ, Inst Med Genet, Cardiff CF14 4XN, Wales. Univ Glasgow, Dept Med Psychol, Gartnavel Royal Hosp, Glasgow, Lanark, Scotland. Univ Edinburgh, Med Stat Unit, Edinburgh, Midlothian, Scotland. Univ Wales Hosp, Cardiff, Wales. RP Archer, HL (reprint author), Cardiff Univ, Inst Med Genet, Heath Pk, Cardiff CF14 4XN, Wales. 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Intell. Disabil. Res. PD MAY PY 2006 VL 50 BP 386 EP 394 DI 10.1111/j.1365-2788.2005.00786.x PN 5 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 038MT UT WOS:000237226600007 PM 16629931 ER PT J AU Talebizadeh, Z Lam, DY Theodoro, MF Bittel, DC Lushington, GH Butler, MG AF Talebizadeh, Z Lam, DY Theodoro, MF Bittel, DC Lushington, GH Butler, MG TI Novel splice isoforms for NLGN3 and NLGN4 with possible implications in autism SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID GENE-EXPRESSION; ALLELIC VARIATION; NEUROLIGIN GENES; EF-HAND; MUTATIONS; ACETYLCHOLINESTERASE; INACTIVATION; NEUREXINS; RECEPTOR; BINDING AB Objective: To screen cDNA for NLGN3 and NLGN4 from lymphoblastoid cells from autistic subjects. Methods and results: 10 young autistic females and 30 nonautistic subjects were studied for alterations in two X linked genes, NLGN3 and NLGN4. A novel NLGN4 isoform lacking exon 4, which occurred de novo on the paternal allele, was identified in one of the autistic females. Monoallelic expression of NLGN4 was seen in this subject and in 11 of 14 informative autistic and non-autistic females using a single nucleotide polymorphism found at 39 UTR. Additionally, the NLGN3 transcript was present in two isoforms (with and without exon 7) in nine of 10 autistic females and in 30 non-autistic subjects, including parents of the autistic female having only the complete transcript with exon 7, and from the whole brain of a control. The novel truncated NLGN3 product may have a regulatory role, as reported in other proteins (for example, vasopressin receptor) by attenuating the function of the full length isoform, resulting in a reduction of the mature protein. Three dimensional protein structures were characterised using comparative modelling, and significant changes were suggested in the protein cores for these two neuroligin isoforms. Conclusions: Splice variants may lead to potentially abnormal neuroligins in the causation of autism spectrum disorders. C1 Univ Missouri, Sect Med Genet & Mol Med, Childrens Mercy Hosp & Clin, Sch Med, Kansas City, MO 64108 USA. Univ Kansas, Mol Graph & Modeling Lab, Lawrence, KS 66045 USA. RP Butler, MG (reprint author), Univ Missouri, Sect Med Genet & Mol Med, Childrens Mercy Hosp & Clin, Sch Med, 2401 Gilham Rd, Kansas City, MO 64108 USA. 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Med. Genet. PD MAY PY 2006 VL 43 IS 5 AR e21 DI 10.1136/jmg.2005.036897 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 037JX UT WOS:000237144100019 PM 16648374 ER PT J AU Vincent, JB Horike, SI Choufani, S Paterson, AD Roberts, W Szatmari, P Weksberg, R Fernandez, B Scherer, SW AF Vincent, JB Horike, SI Choufani, S Paterson, AD Roberts, W Szatmari, P Weksberg, R Fernandez, B Scherer, SW TI An inversion inv(4)(p12-p15.3) in autistic siblings implicates the 4p GABA receptor gene cluster SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID SUBUNIT GENES; ASSOCIATION; LINKAGE; DISORDER; EXPRESSION; FAMILY AB Introduction: We describe the case of two brothers diagnosed with autism who both carry a paracentic inversion of the short arm of chromosome 4 (46, XY, inv(4)(p12-p15.3)). We have determined that this inversion is inherited from an apparently unaffected mother and unaffected maternal grandfather. Methods/Results: Using fluorescence in situ hybridisation analysis and Southern blot hybridisation we identified the breakpoints. The proximal breakpoint (4p12) maps to a region containing a cluster of gamma-aminobutyric acid A (GABA(A)) receptor genes, and directly interrupts the GABRG1 gene, the distal-most gene of the cluster. We also identified an insertion/deletion polymorphism for a similar to 2 kb LINE1 (L1) element that occurs within intron 7 of GABRG1. Our genotype analysis amongst autism families indicated that the L1 deletion allele did not show increased transmission to affected individuals. No linkage disequilibrium was evident between the L1 and single nucleotide polymorphisms in adjacent GABA(A) receptor genes on 4p, where a recent study has identified significant association with autism. Discussion: Despite this, the identification of an inversion breakpoint disrupting GABRG1 provides solid support for the genetic involvement of the short arm of chromosome 4 in the genetic aetiology of autism, and for the hypothesis of disrupted GABA neurotransmission in autism. C1 Hosp Sick Children, Program Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Ctr Addict & Mental Hlth, Neurogenet Sect, Toronto, ON, Canada. Hosp Sick Children, Autism Res Unit, Toronto, ON M5G 1X8, Canada. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. Hosp Sick Children, Div Clin & Metab Genet, Toronto, ON M5G 1X8, Canada. Mem Univ Newfoundland, Discipline Genet, Hlth Sci Ctr, St John, NF, Canada. RP Scherer, SW (reprint author), Hosp Sick Children, Program Genet & Genom Biol, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. EM swscherer@sickkids.ca RI Paterson, Andrew/A-4088-2011; Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013 OI Paterson, Andrew/0000-0002-9169-118X; Scherer, Stephen /0000-0002-8326-1999 CR Barnard EA, 1998, PHARMACOL REV, V50, P291 Barrett JC, 2005, BIOINFORMATICS, V21, P263, DOI 10.1093/bioinformatics/bth457 Blatt GJ, 2001, J AUTISM DEV DISORD, V31, P537, DOI 10.1023/A:1013238809666 Buxbaum JD, 2002, MOL PSYCHIATR, V7, P311, DOI 10.1038/sj/mp/4001011 Chang YC, 1996, J NEUROSCI, V16, P5415 Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Dhossche Dirk, 2002, Med Sci Monit, V8, pPR1 Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 Han JS, 2004, NATURE, V429, P268, DOI 10.1038/nature02536 Horvath S, 2004, GENET EPIDEMIOL, V26, P61, DOI 10.1002/gepi.10295 Iafrate AJ, 2004, NAT GENET, V36, P949, DOI 10.1038/ng1416 Gibbs RA, 2003, NATURE, V426, P789, DOI 10.1038/nature02168 Bailey A, 1998, HUM MOL GENET, V7, P571 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Ma DQ, 2005, AM J HUM GENET, V77, P377, DOI 10.1086/433195 McCauley JL, 2004, AM J MED GENET B, V131B, P51, DOI 10.1002/ajmg.b.30038 MEDNE L, 2003, AM J HUM GENET, V73, pA847 Menold MM, 2001, J NEUROGENET, V15, P245 Muotri AR, 2005, NATURE, V435, P903, DOI 10.1038/nature03663 NAYEEM N, 1994, J NEUROCHEM, V62, P815 Nurmi EL, 2003, MOL PSYCHIATR, V8, P624, DOI 10.1038/sj.mp.4001283 Ostertag EM, 2001, ANNU REV GENET, V35, P501, DOI 10.1146/annurev.genet.35.102401.091032 Sabaratnam M, 2000, EUR CHILD ADOLES PSY, V9, P307 SCHOFIELD PR, 1987, NATURE, V328, P221, DOI 10.1038/328221a0 XU J, 2004, CURR GENOMICS, V4, P347 NR 26 TC 26 Z9 27 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD MAY PY 2006 VL 43 IS 5 BP 429 EP 434 DI 10.1136/jmg.2005.039693 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 037JX UT WOS:000237144100009 PM 16556609 ER PT J AU Afzal, MA Ozoemena, LC O'Hare, A Kidger, KA Bentley, ML Minor, PD AF Afzal, MA Ozoemena, LC O'Hare, A Kidger, KA Bentley, ML Minor, PD TI Absence of detectable measles virus genome sequence in blood of autistic children who have had their MMR vaccination during the routine childhood immunization schedule of UK SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE real-time quantitative RT-PCR; measles virus; autism ID INFLAMMATORY-BOWEL-DISEASE; RUBELLA VACCINE; MUMPS; PCR; DISORDER; ASSAY; GENE; RNA AB Leukocyte preparations from children with documented evidence of MMR vaccination and confirmed diagnosis of autism were examined by several assays designed to target multiple regions of the measles virus genome sequence. No sample was found positive by any method. The assays applied were highly sensitive, specific and robust in nature, and were based on the amplification of measles virus RNA transcripts by real-time quantitative RT-PCR (QRT-PCR) as well as by conventional RT-PCR-nested PCR. The assays applied were potentially able to detect measles virus RNA down to single figure copy numbers per reaction. The amount of total nucleic acid extract of leukocytes subjected to various measles virus-specific investigations was several fold higher than minimally required of a sample where measles virus persistence is well documented. This study failed to substantiate reports of the persistence of measles virus in autistic children with development regression. (c) 2006 Wiley-Liss, Inc. C1 Natl Inst Biol Stand & Controls, Div Virol, Potters Bar EN6 3QG, Herts, England. Univ Edinburgh, Dept Reprod & Dev Sci, Edinburgh, Midlothian, Scotland. RP Afzal, MA (reprint author), Natl Inst Biol Stand & Controls, Div Virol, Blanche Lane S Mimms, Potters Bar EN6 3QG, Herts, England. 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Med. Virol. PD MAY PY 2006 VL 78 IS 5 BP 623 EP 630 DI 10.1002/jmv.20585 PG 8 WC Virology SC Virology GA 030TH UT WOS:000236657000014 PM 16555271 ER PT J AU Tonge, B Brereton, A Kiomall, M Mackinnon, A King, N Rinehart, N AF Tonge, B Brereton, A Kiomall, M Mackinnon, A King, N Rinehart, N TI Effects on parental mental health of an education and skills training program for parents of young children with autism: A randomized controlled trial SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; parents; early intervention ID FAMILY ASSESSMENT DEVICE; PSYCHIATRIC-DISORDERS; INTERVENTION; DISABILITIES; INDIVIDUALS; DEPRESSION; SYMPTOMS; MOTHERS; FUTURE AB Objective: To determine the impact of a parent education and behavior management intervention (PEBM) on the mental health and adjustment of parents with preschool children with autism. Method: A randomized, group-comparison design involving a parent education and counseling intervention to control for nonspecific therapist effects and a control sample was used. Two metropolitan and two rural regions were randomly allocated to intervention groups (n = 70) or control (n = 35). The parents of consecutive children with autism (2(1)/(2)-5 years old) from the autism assessment services for the intervention regions were then randomly allocated to either a 20-week manual-based parent education and behavior management intervention (n = 35) or a manual-based parent education and counseling intervention (n = 35). The main outcome measure of parental mental health was the General Health Questionnaire used pre- and postintervention and at 6-month follow-up. Results: Both treatments resulted in significant and progressive improvement in overall mental health at follow-up (F = 2, 97, p = .007) and mental health significantly improved over time in the 54% of principal caregivers who had the highest levels of mental health problems. The parent education and behavior management intervention was effective in alleviating a greater percentage of anxiety, insomnia, and somatic symptoms and family dysfunction than parent education and counseling at 6-month follow-up. Conclusions: A 20-week parent education and skills training program for parents of young children newly diagnosed with autism provides significant improvements in parental mental health and adjustment, justifying its addition to early intervention programs at least for parents with mental health problems. C1 Monash Univ, Ctr Dev Psychiat & Psychol, Monash Med Ctr, Clayton, Vic 3168, Australia. Monash Univ, Ctr Dev Psychiat, Clayton, Vic 3168, Australia. 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Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 2006 VL 45 IS 5 BP 561 EP 569 DI 10.1097/01.chi.0000205701.48324.26 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 036TM UT WOS:000237098400007 PM 16670650 ER PT J AU Mostofsky, SH Dubey, P Jerath, VK Jansiewicz, EM Goldberg, MC Denckla, MB AF Mostofsky, SH Dubey, P Jerath, VK Jansiewicz, EM Goldberg, MC Denckla, MB TI Developmental dyspraxia is not limited to imitation in children with autism spectrum disorders SO JOURNAL OF THE INTERNATIONAL NEUROPSYCHOLOGICAL SOCIETY LA English DT Article DE praxis; apraxia; motor skills; imitation; gesture; Asperger's ID DIAGNOSTIC OBSERVATION SCHEDULE; INFANTILE-AUTISM; CORTICOBASAL DEGENERATION; ASPERGERS-SYNDROME; IDEOMOTOR APRAXIA; MOTOR IMPAIRMENT; LIMB APRAXIA; TASK DEMANDS; DEFICITS; BEHAVIOR AB Impaired imitation of skilled gestures is commonly reported in autism. Questions, however, remain as to whether impaired imitation is associated with a more generalized deficit in performance of gestures consistent with a dyspraxia and whether the pattern of errors differs from that observed in typically developing children. To address these questions, praxis in 21 high-functioning children with autism spectrum disorders (ASD) was compared with 24 typically developing controls using a traditional approach in which performance was evaluated through detailed examination of error types. Children with ASD produced significantly fewer correct responses not only during Gesture to Imitation, but also during Gesture to Command and with Tool Use. The pattern of errors in ASD was similar to that of controls with spatial errors being most common in both groups; however, body-part-for-tool errors were more common in children with ASD, suggesting dyspraxia is not entirely attributable to motor deficits. The findings suggest that autism is associated with a generalized praxis deficit, rather than a deficit specific to imitation. In a developmental disorder such as autism, the findings may reflect abnormalities in frontal/parietal-subcortical circuits important for acquisition (i.e., learning) of sensory representations of movement and/or the motor sequence programs necessary to execute them. C1 Johns Hopkins Univ, Sch Med, Dept Dev Cognit Neurol, Kennedy Krieger Inst, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, FM Kirby Res Ctr, Kennedy Krieger Inst, Baltimore, MD 21205 USA. RP Mostofsky, SH (reprint author), Johns Hopkins Univ, Sch Med, Dept Dev Cognit Neurol, Kennedy Krieger Inst, 707 N Broadway, Baltimore, MD 21205 USA. 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PD MAY PY 2006 VL 11 IS 5 BP 424 EP 424 DI 10.1038/sj.mp.4001826 PG 1 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 036FX UT WOS:000237057800001 PM 16636689 ER PT J AU Yirmiya, N Rosenberg, C Levi, S Salomon, S Shulman, C Nemanov, L Dina, C Ebstein, RP AF Yirmiya, N Rosenberg, C Levi, S Salomon, S Shulman, C Nemanov, L Dina, C Ebstein, RP TI Association between the arginine vasopressin 1a receptor (AVPR1a) gene and autism in a family-based study: mediation by socialization skills SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; arginine vasopressin receptor 1a (AVPR1a); candidate gene; transmission disequilibrium; social adjustment; polymorphism ID POLYMORPHISMS; BEHAVIOR; MICROSATELLITE; PROMOTER; TESTS AB We examined three microsatellites in the arginine vasopressin 1a receptor gene (AVPR1a), two in the promoter region (RS1 and RS3) and an intronic microsatellite (AVR), for association with autism as well as scores on the Vineland Adaptive Behavior Scale (VABS), the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Scale-Generic (ADOS-G), measures that are widely used to diagnose autism spectrum disorders. We tested for association between the AVPR1a microsatellites and autism in 116 families (128 probands diagnosed with the ADI-R and ADOS-G using a family-based association test (UNPHASED)). Testing each individual microsatellite showed significant transmission disequilibrium in these families with the AVR intronic microsatellite (UNPHASED: LRS = 11.46, global P-value = 0.009, df = 3). Haplotype analysis of three microsatellites also showed significant association (LRS = 144.94, df = 103, global P = 0.004). Additionally, significant association is observed between these three microsatellite haplotypes and the VABS scores (P = 0.009), with the ADI-R (P = 0.009) and the ADOS-G (P = 0.0000765) diagnoses of autistic disorder versus pervasive developmental disorder-not otherwise specified (PDD-NOS) that were available for 47 of these probands. This is the third consecutive report of an association between the AVPR1a gene and autism spectrum disorders and in the current study a third microsatellite is shown to be associated with autism spectrum disorders as well as haplotypes consisting of all three markers. Importantly, the association appears to be mainly mediated by the role of the AVPR1a gene in shaping socialization skills, similar to its role in lower vertebrates. C1 Hebrew Univ Jerusalem, Dept Psychol, Scheinfeld Ctr Human Genet Social Sci, IL-91905 Jerusalem, Israel. S Herzog Mem Hosp, IL-91905 Jerusalem, Israel. Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Child Psychiat, IL-91905 Jerusalem, Israel. Hebrew Univ Jerusalem, Sch Social Work, IL-91905 Jerusalem, Israel. Inst Biol, Lille, France. RP Ebstein, RP (reprint author), Hebrew Univ Jerusalem, Dept Psychol, Scheinfeld Ctr Human Genet Social Sci, IL-91905 Jerusalem, Israel. 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SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE anxiety disorder; nosology; obsessive compulsive disorder (OCD); obsessive-compulsive spectrum ID POSTTRAUMATIC-STRESS-DISORDER; CEREBRAL BLOOD-FLOW; SEROTONIN REUPTAKE INHIBITOR; BODY DYSMORPHIC DISORDER; HOPKINS OCD FAMILY; PANIC DISORDER; SPECTRUM DISORDERS; GENERALIZED ANXIETY; ANOREXIA-NERVOSA; DOUBLE-BLIND AB Obsessive-compulsive disorder (OCD) is classified as an anxiety disorder in the DSM-IV-TR [American Psychiatric Association, 2000. Diagnostic and statistical manual of mental disorders, Fourth ed., rev. Washington, DC: Author]; however, the notion of a spectrum of obsessive-compulsive (OC) related disorders that is comprised of such disparate disorders as OCD, body dysmorphic disorder, certain eating disorders, pathological gambling, and autism, is gaining acceptance. The fact that these disorders share obsessive-compulsive features and evidence similarities in patient characteristics, course, comorbidity, neurobiology, and treatment response raises the question of whether OCD is best conceptualized as an anxiety or an OC spectrum disorder. This article reviews evidence from comorbidity and family studies, as well as biological evidence related to neurocircuitry, neurotransmitter function, and pharmacologic treatment response that bear on this question. The implications of removing OCD from the anxiety disorders category and moving it to an OC spectrum disorders category, as is being proposed for the DSM-V, is discussed. (c) 2005 Elsevier Inc. All rights reserved. C1 CUNY Mt Sinai Sch Med, New York, NY 10029 USA. RP Bartz, JA (reprint author), CUNY Mt Sinai Sch Med, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA. 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NEURO-PSYCHOPH JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry PD MAY PY 2006 VL 30 IS 3 BP 338 EP 352 DI 10.1016/j.pnpbp.2005.11.003 PG 15 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 037LW UT WOS:000237149400003 PM 16455175 ER PT J AU McCabe, T AF McCabe, T TI My brother's keeper: A kindergartner's view of autism SO PSYCHIATRIC SERVICES LA English DT Book Review CR RICHARDS J, 2005, MY BROTHERS KEEPER K NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD MAY PY 2006 VL 57 IS 5 BP 745 EP 745 DI 10.1176/appi.ps.57.5.745 PG 1 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 039JJ UT WOS:000237301500061 ER PT J AU Lam, KSL Aman, MG Arnold, LE AF Lam, KSL Aman, MG Arnold, LE TI Neurochemical correlates of autistic disorder: A review of the literature SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Review DE autism; neurochemical investigations; neurotransmitters; serotonin; dopamine; norepinepherine; acetylcholine; oxytocin; endogenous opioids; cortisol; glutamate; gamma-aminobutyric acid ID PERVASIVE DEVELOPMENTAL DISORDERS; PLASMA BETA-ENDORPHIN; DEXAMETHASONE SUPPRESSION TEST; EARLY INFANTILE-AUTISM; SEROTONIN TRANSPORTER 5-HTT; WHOLE-BLOOD SEROTONIN; CEREBROSPINAL-FLUID; DOUBLE-BLIND; HOMOVANILLIC-ACID; 5-HYDROXYINDOLEACETIC ACID AB Review of neurochemical investigations in autistic disorder revealed that a wide array of transmitter systems have been studied, including serotonin, dopamine, norepinephrine, acetylcholine, oxytocin, endogenous opioids, cortisol, glutamate, and gamma-aminobutyric acid (GABA). These studies have been complicated by the fact that autism is a very heterogeneous disorder which often presents with comorbid behavioral problems. In addition, many of these studies employed very small samples and inappropriate control groups, making it difficult to draw conclusions with confidence. Overall, serotonin appears to have the most empirical evidence for a role in autism, but this requires further investigation and replication. There is little support for the notion that a dysfunction of norepinephrine or the endogenous opioids are related to autism. The role of dopaminergic functioning has not been compelling thus far, though conflicting findings on central dopamine turnover require further study. Promising new areas of study may include possible dysfunction of the cholinergic system, oxytocin, and amino acid neurotransmitters. Implications for pharmacotherapy are briefly discussed for each neurotransmitter system with brief research examples. Review of this work emphasizes the need for future studies to control for subject variables, such as race, sex, pubertal status, and distress associated with blood draws, which can affect measures of neurochemical function. In addition, research in neurochemistry must continue to work in concert with other subspecialties to form a more comprehensive and theory-based approach to the neurobiological correlates of autistic disorder. (c) 2005 Elsevier Ltd. All rights reserved. C1 Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC USA. RP Aman, MG (reprint author), Ohio State Univ, Nisonger Ctr, 1581 Dodd Dr, Columbus, OH 43210 USA. 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Dev. Disabil. PD MAY-JUN PY 2006 VL 27 IS 3 BP 254 EP 289 DI 10.1016/j.ridd.2005.03.003 PG 36 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 042LO UT WOS:000237529700003 PM 16002261 ER PT J AU Bosa, CA AF Bosa, CA TI Autism: psychoeducational intervention SO REVISTA BRASILEIRA DE PSIQUIATRIA LA Portuguese DT Article DE autistic disorder/therapy; disease management; family/complications; identification (psychology); early intervention (education) ID SPECTRUM DISORDERS; YOUNG-CHILDREN; FOLLOW-UP; STRESS; COMMUNICATION; FAMILIES; PARENTS AB There is increasing recognition about the importance of taking into account both child and family needs when treating autism. However it has been a major debate about what intervention is the most appropriate. In this paper we will review the current literature on the different interventions that have been used in the treatment of autism with special attention to those that are empirically based. It is not our objective to discuss in detail any particular intervention. We intend to present an overview of both positive aspects and limitations of different interventions. The conclusion is that there is no single approach that is totally effective for all children the whole time. Instead, it is argued that families change their expectation and values regarding their children's treatment according to the child's development and the family context. In other words, a specific intervention that may work well in a certain period of time (e.g. pre-school years) may not work so well in the following years (e.g. adolescence). Finally the importance of early identification and treatment of autism is stressed. C1 UFRGS, Inst Psicol, BR-90035003 Porto Alegre, RS, Brazil. RP Bosa, CA (reprint author), UFRGS, Inst Psicol, Ramiro Barcelos 2-600, BR-90035003 Porto Alegre, RS, Brazil. 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Bras. Psiquiatr. PD MAY PY 2006 VL 28 SU 1 BP S29 EP S38 DI 10.1590/S1516-44462006000500005 PG 10 WC Psychiatry SC Psychiatry GA 047AM UT WOS:000237852200005 PM 16791389 ER PT J AU Kiln, A AF Kiln, A TI Autism and Asperger syndrome: an overview SO REVISTA BRASILEIRA DE PSIQUIATRIA LA Portuguese DT Article DE autism/therapy; Asperger syndrome/therapy; psychopharmacology/standards; child development/drug effects; disease management ID DISORDER AB Autism and Asperger syndrome are diagnostic entities in a family of neurodevelopmental disorders disrupting fundamental processes of socialization, communication and learning, collectively known as pervasive developmental disorders. This group of conditions is among the most common developmental disorders, affecting 1 in every 200 or so individuals. They are also the most strongly genetically related among developmental disorders, with recurrence risks within sibships of the order of 2 to 15% if a broader definition of affectedness is adopted. Their early onset, symptom profile, and chronicity implicate fundamental biological mechanisms involved in social adaptation. Advances in their understanding are leading to a new social neuroscience perspective of normative socialization processes and specific disruptions thereof These processes may lead to the emergence of the highly heterogeneous phenotypes associated with autism, the paradigmatic pervasive developmental disorder, and its variants. This overview focuses on the history, nosology, and the clinical and associated features of the two most well-known pervasive developmental disorders autism and Asperger syndrome. C1 Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT 06520 USA. RP Kiln, A (reprint author), Yale Univ, Sch Med, Yale Child Study Ctr, 230 S Frontage Rd, New Haven, CT 06520 USA. 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PD MAY PY 2006 VL 28 SU 1 BP S3 EP S11 PG 9 WC Psychiatry SC Psychiatry GA 047AM UT WOS:000237852200002 ER PT J AU Klin, A Mercadante, MT AF Klin, A Mercadante, MT TI Autism and the pervasive developmental disorders SO REVISTA BRASILEIRA DE PSIQUIATRIA LA Portuguese DT Editorial Material CR BOSA CA, 2006, REV BRAS PSIQUIAT S1, V28, P48 GUPTA AR, 2006, REV BRAS PSIQUIAT S1, V28, P30 Klin A, 2006, REV BRAS PSIQUIATR, V28, P3 MERCADANTE MT, 2006, REV BRAS PSIQUIAT S1, V28, P13 NIKOLOV R, 2006, REV BRAS PSIQUIAT S1, V28, P40 ZIBOVICIUS M, 2006, REV BRAS PSIQUIAT S1, V28, P22 NR 6 TC 2 Z9 3 PU ASSOCIACAO BRASILEIRA DE PSIQUIATRIA PI SAO PAULO PA SUBSCRIPTION DEPARTMENT, RUA PEDRO DE TOLEDO, 967 - CASA 01, SAO PAULO, SP, BRAZIL SN 1516-4446 J9 REV BRAS PSIQUIATR JI Rev. Bras. Psiquiatr. PD MAY PY 2006 VL 28 SU 1 BP S1 EP S2 DI 10.1590/S1516-44462006000500001 PG 2 WC Psychiatry SC Psychiatry GA 047AM UT WOS:000237852200001 PM 16791386 ER PT J AU Nikolov, R Jonker, J Scahill, L AF Nikolov, R Jonker, J Scahill, L TI Autistic disorder: current psychopharmacological treatments and areas of interest for future developments SO REVISTA BRASILEIRA DE PSIQUIATRIA LA Portuguese DT Article DE autistic disorder; antipsychotic agents; anticonvulsants; antidepressant agents; disease management ID PLACEBO-CONTROLLED TRIAL; OPEN-LABEL; MENTAL-RETARDATION; DOUBLE-BLIND; BEHAVIORAL SYMPTOMS; INFANTILE-AUTISM; CLINICAL-TRIAL; SELF-INJURY; CHILDREN; OLANZAPINE AB Autistic disorder and the group of related conditions defined as pervasive developmental disorders are chronic neurodevelopmental disorders starting in early childhood and affecting a significant number of children and families. Although the causes and much of the pathophysiology of the disorder remain unknown, in recent years a number of available medication treatments have been identified as holding promise in alleviating some of the most disabling maladaptive behaviors, associated with pervasive developmental disorders. However these treatments do not address the core symptoms of the disease and oftentimes their side effects outweigh their benefits. Therefore there is substantial need for new medications that are safer and more effective in addressing the behavior symptoms of autism. The aim of this review is to highlight the available current pharmacotherapies and those emerging treatments with potential to enhance the treatment options of patients with pervasive developmental disorders. C1 Yale Univ, Yale Child Study Ctr, Sch Med, Sch Nursing, New Haven, CT 06520 USA. Univ Groningen, Groningen, Netherlands. RP Nikolov, R (reprint author), Yale Univ, Yale Child Study Ctr, Sch Med, Sch Nursing, 230 S Frontage Rd,POB 207900, New Haven, CT 06520 USA. 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Bras. Psiquiatr. PD MAY PY 2006 VL 28 SU 1 BP S39 EP S46 DI 10.1590/S1516-44462006000500006 PG 8 WC Psychiatry SC Psychiatry GA 047AM UT WOS:000237852200006 PM 16791391 ER PT J AU Zilbovicius, M Meresse, I Boddaert, N AF Zilbovicius, M Meresse, I Boddaert, N TI Autism: neuroimaging SO REVISTA BRASILEIRA DE PSIQUIATRIA LA Portuguese DT Article DE autistic syndrome; magnetic resonance imaging; tomography,emission-computed; acoustic stimulation; auditive perception ID CEREBRAL-BLOOD-FLOW; VOXEL-BASED MORPHOMETRY; FUSIFORM FACE AREA; CHILDHOOD AUTISM; CORPUS-CALLOSUM; SPECTRUM DISORDER; ASPERGER-SYNDROME; COMPLEX SOUNDS; BRAIN; MRI AB Autism is a neurodevelopmental disorder with a range of clinical presentations. These presentations vary from mild to severe and are referred to as autism spectrum disorders. The most common clinical sign of autism spectrum disorders is social interaction impairment, which is associated with verbal and non-verbal communication deficits and stereotyped and repetitive behaviors. Thanks to recent brain imaging studies, scientists are getting a better idea of the neural circuits involved in autism spectrum disorders. Indeed, functional brain imaging, such as positron emission tomography, single foton emission tomography and functional MRI have opened a new perspective to study normal and pathological brain functioning. Three independent studies have found anatomical and rest functional temporal lobe abnormalities in autistic patients. These alterations are localized in the superior temporal sulcus bilaterally, an area which is critical for perception of key social stimuli. In addition, functional studies have shown hypoactivation of most areas implicated in social perception (face and voice perception) and social cognition (theory of mind). These data suggest an abnormal functioning of the social brain network in autism. The understanding of the functional alterations of this important mechanism may drive the elaboration of new and more adequate social re-educative strategies for autistic patients. C1 Serv Hosp Frederic Joliot, ERM 0205, INSERM, CEA, F-91406 Orsay, France. CHU Necker Enfants Malad, Serv Radiol Pediat, Paris, France. Univ Paris 05, Paris, France. RP Zilbovicius, M (reprint author), Serv Hosp Frederic Joliot, ERM 0205, INSERM, CEA, 4 Pl Gen Leclerc, F-91406 Orsay, France. 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With the exception of more tics, cardiac surgery was associated with positive behaviors: less withdrawn behavior, better mood, and a more easy temperament. Tube feeding was also related to positive behavior, since participants with a history Of tube Feeding showed less intense behavior. Cerebral deficits were associated with three problem behaviors: more intense and withdrawn behavior and a worse mood. Deafblindness was associated with developmental delays in expressive and overall communication level, and recurrent middle ear infections correlated with delays in written language. Of all medical conditions, only the presence or absence of heart defects and cardiac surgery could differentiate between the participants with regard to the number of behavioral problems. participants with heart surgery especially, had less behavior problems. The number of operations and hospitalizations,vas not associated with behavior, but the total length of the hospitalizations was. Long hospital stays were associated with less problem behavior, especially internalizing behaviors. Cerebral and heart problems did not result in longer hospital stays, whereas esophageal reflux did. Age effects were reflected in older participants, who showed more internalizing problems. Heart surgery and hospitalization may be protective factors, but the protection might not be the actual surgery or hospital stay, as there may be other variables that are the actual cause, such as reduced vitality or altered parent child interactions after heart surgery. The study could not confirm a significant association between medical conditions and autism found in previous studies. (c) 2006 Wiley-Liss, Inc. C1 Radboud Univ Nijmegen, Dept Special Educ, NL-6500 HE Nijmegen, Netherlands. Radboud Univ Nijmegen, Med Ctr, Dept Otorhinolaryngol, Nijmegen, Netherlands. Radboud Univ Nijmegen, Med Ctr, Dept Med Genet, Nijmegen, Netherlands. Viataal, Inst Deaf, St Michielsgestel, Netherlands. RP Vervloed, MPJ (reprint author), Radboud Univ Nijmegen, Dept Special Educ, Montessorilaan 3,POB 9104, NL-6500 HE Nijmegen, Netherlands. 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